Archive for the ‘Cardiac Stem Cells’ Category

Keeping in tradition with the Us commitment to advance the fields of medicine and surgery, our physicians are focusing on regenerative medicine as the next frontier in treating cardiovascular disease. Researchers within the Cardiovascular Center estimate cell therapy will be FDA-approved within three years. The goal of this therapy is to give cells back to the heart in order for it to grow stronger, work harder, and function more like a younger heart. Currently, studies include the potentiality of injecting cardiac repair cells into patients hearts to improve function.

This is the first trial of its kind in the United States, providing heart patients who have limited or no other options with a viable treatment. Using some of the best imaging technology, researchers have been able to see improvements in patients within six months after injecting their own cells directly into the left ventricle of the heart during minimally invasive surgery.

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Heart Stem Cell Therapy | University of Utah Health Care

A new method for delivering stem cells to damaged heart muscle has shown early promise in treating severe heart failure, researchers report.

In a preliminary study, they found the tactic was safe and feasible for the 48 heart failure patients they treated. And after a year, the patients showed a modest improvement in the heart's pumping ability, on average.

It's not clear yet whether those improvements could be meaningful, said lead researcher Dr. Amit Patel, director of cardiovascular regenerative medicine at the University of Utah.

He said larger clinical trials are underway to see whether the approach could be an option for advanced heart failure.

Other experts stressed the bigger picture: Researchers have long studied stem cells as a potential therapy for heart failure -- with limited success so far.

"There's been a lot of promise, but not much of a clinical benefit yet," said Dr. Lee Goldberg, who specializes in treating heart failure at the University of Pennsylvania.

Researchers are still sorting through complicated questions, including how to best get stem cells to damaged heart muscle, said Goldberg, who was not involved in the new study.

What's "novel" in this research, he said, is the technique Patel's team used to deliver stem cells to the heart. They took stem cells from patients' bone marrow and infused them into the heart through a large vein called the coronary sinus.

Patel agreed that the technique is the advance.

"Most other techniques have infused stem cells through the arteries," Patel explained. One obstacle, he said, is that people with heart failure generally have hardened, narrowed coronary arteries, and the infused stem cells "don't always go to where they should."

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Stem Cells Show Promise in Heart Failure Treatment

For immediate release: September 10, 2012

Baltimore, MD --Researchers at the University of Maryland School of Medicine, who are exploring novel ways to treat serious heart problems in children, have conducted the first direct comparison of the regenerative abilities of neonatal and adult-derived human cardiac stem cells. Among their findings: cardiac stem cells (CSCs) from newborns have a three-fold ability to restore heart function to nearly normal levels compared with adult CSCs. Further, in animal models of heart attack, hearts treated with neonatal stem cells pumped stronger than those given adult cells. The study is published in the September 11, 2012, issue of Circulation.

The surprising finding is that the cells from neonates are extremely regenerative and perform better than adult stem cells, says the study's senor author, Sunjay Kaushal, M.D., Ph.D., associate professor of surgery at the University of Maryland School of Medicine and director, pediatric cardiac surgery at the University of Maryland Medical Center. We are extremely excited and hopeful that this new cell-based therapy can play an important role in the treatment of children with congenital heart disease, many of whom don't have other options.

Dr. Kaushal envisions cellular therapy as either a stand-alone therapy for children with heart failure or an adjunct to medical and surgical treatments. While surgery can provide structural relief for some patients with congenital heart disease and medicine can boost heart function up to two percent, he says cellular therapy may improve heart function even more dramatically. We're looking at this type of therapy to improve heart function in children by 10, 12, or 15 percent. This will be a quantum leap in heart function improvement.

Heart failure in children, as in adults, has been on the rise in the past decade and the prognosis for patients hospitalized with heart failure remains poor. In contrast to adults, Dr. Kaushal says heart failure in children is typically the result of a constellation of problems: reduced cardiac blood flow; weakening and enlargement of the heart; and various congenital malformations. Recent research has shown that several types of cardiac stem cells can help the heart repair itself, essentially reversing the theory that a broken heart cannot be mended.

Stem cells are unspecialized cells that can become tissue- or organ-specific cells with a particular function. In a process called differentiation, cardiac stem cells may develop into rhythmically contracting muscle cells, smooth muscle cells or endothelial cells. Stem cells in the heart may also secrete growth factors conducive to forming heart muscle and keeping the muscle from dying.

To conduct the study, researchers obtained a small amount of heart tissue during normal cardiac surgery from 43 neonates and 13 adults. The cells were expanded in a growth medium yielding millions of cells. The researchers developed a consistent way to isolate and grow neonatal stem cells from as little as 20 milligrams of heart tissue. Adult and neonate stem cell activity was observed both in the laboratory and in animal models. In addition, the animal models were compared to controls that were not given the stem cells.

Dr. Kaushal says it is not clear why the neonatal stem cells performed so well. One explanation hinges on sheer numbers: there are many more stem cells in a baby's heart than in the adult heart. Another explanation: neonate-derived cells release more growth factors that trigger blood vessel development and/or preservation than adult cells.

This research provides an important link in our quest to understand how stem cells function and how they can best be applied to cure disease and correct medical deficiencies, says E. Albert Reece, M.D., Ph.D., M.B.A., vice president for medical affairs, University of Maryland; the John Z. and Akiko K. Bowers Distinguished Professor; and dean, University of Maryland School of Medicine. Sometimes simple science is the best science. In this case, a basic, comparative study has revealed in stark terms the powerful regenerative qualities of neonatal cardiac stem cells, heretofore unknown.

Insights gained through this research may provide new treatment options for a life-threatening congenital heart syndrome called hypoplastic left heart syndrome (HLHS). Dr. Kaushal and his team will soon begin the first clinical trial in the United States to determine whether the damage to hearts of babies with HLHS can be reversed with stem cell therapy. HLHS limits the heart's ability to pump blood from the left side of the heart to the body. Current treatment options include either a heart transplant or a series of reconstructive surgical procedures. Nevertheless, only 50-60 percent of children who have had those procedures survive to age five.

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Cardiac Stem Cells (CSCs) | University of Maryland Medical ...

Stem Cell Clinical Research & Deployment Cardiovascular & Pulmonary Conditions

The Manhattan Regenerative Medicine Medical Group is proud to be part of the only Institutional Review Board (IRB)-based stem cell treatment network in the United States that utilizes fat-transfer surgical technology. The Manhattan Regenerative Medicine Medical Group offers IRB approved protocols and investigational use ofAdult Autologous Adipose-derived Stem Cells (ADSCs) for clinical research and deployment for numerous Cardiovascular and Pulmonary disorders, inclusive of:

Cardiovascular conditions include medical problems involving the heart and vascular system (the arterial and venous blood vessels). The most common cardiovascular condition is atherosclerotic coronary artery disease (ASCVD), which especially affects the coronary arteries and is the leading cause of heart attacks and death worldwide; and Congestive Heart Failure (CHF).

Other common cardiovascular conditions involve the cardiac muscle (CHF), cardiac valves, and heart rhythm. Many patients are typically treated with a multitude of medications; many patients require surgical interventions such as coronary angioplasty, coronary artery bypass, or other surgeries. Often patients, despite maximum therapy with medications and surgery, continue to suffer pain, discomfort, disability and have marked restrictions in their normal daily living activities.

The Manhattan Regenerative Medicine Medical Group is proud to be part of the only Institutional Review Board (IRB)-based stem cell treatment network in the United States that utilizes fat-transfer surgical technology. We have an array of ongoing IRB-approved protocols, andwe provide care for patients with a wide variety of disorders that may be treated with adult stem cell-based regenerative therapy.

The Manhattan Regenerative Medicine Medical Group offers IRB approved protocols and investigational use of Autologous Adult Adipose Derived Stem Cells (ADSCs) for clinical research and deployment for numerous cardiovascular conditions. These ADSCs cells are derived from fat an exceptionally abundant source of stem cells that has been removed during our mini-liposuction office procedure. The source of the regenerative stem cells actually comes from stromal vascular fraction (SVF) a protein rich segment from processed adipose tissue. SVF contains a mononuclear cell line (predominantly autologous mesenchymal stem cells), macrophage cells, endothelial cells, red blood cells, and important growth factors that facilitate the stem cell process and promote their activity. Our technology allows us to isolate high numbers of viable cells that we can deploy during the same surgical setting.

The SVF and stem cells are then deployed back into the patients body via injection or IV infusion on an outpatient basis; the total procedure takes less than two hours; and only local anesthesia is used. Not all cardiovascular problems respond to stem cell therapy, and each patient must be assessed individually to determine the potential for optimal results from this regenerative medicine process.

The Manhattan Regenerative Medicine Medical Group is committed not only to providing a high degree of quality care for our patients with cardiovascular problems but we are also highly committed to clinical stem cell research and the advancement of regenerative medicine. At the Miami Stem Cell Treatment Center we exploit anti-inflammatory, immuno-modulatory and regenerative properties of adult stem cells to mitigate cardiovascular conditions which are otherwise lethal to our bodies.

Myocardial infarction (heart attack) is responsible for significant cardiac muscle destruction and impairment due to ischemia (lack of blood flow). This can lead to further or recurrent restriction of blood flow thereby causing re-current infarct and pain on exertion (or even rest) known as chronic angina. Chronic angina causes restriction of daily activities of everyday living and is plagued with chest pain, chest pressure, and depression. This problem is caused most commonly by coronary artery disease which is very common in the United States and associated with significant morbidity and mortality.

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Cardiovascular Stem Cell Therapy

Abstract

Myocardial infarctioninduced heart failure is a prevailing cause of death in the United States and most developed countries. The cardiac tissue has extremely limited regenerative potential, and heart transplantation for reconstituting the function of damaged heart is severely hindered mainly due to the scarcity of donor organs. To that end, stem cells with their extensive proliferative capacity and their ability to differentiate toward functional cardiomyocytes may serve as a renewable cellular source for repairing the damaged myocardium. Here, we review recent studies regarding the cardiogenic potential of adult progenitor cells and embryonic stem cells. Although large strides have been made toward the engineering of cardiac tissues using stem cells, important issues remain to be addressed to enable the translation of such technologies to the clinical setting.

Heart disease is a significant cause of morbidity and mortality worldwide. In the United States, heart failure is ranked number one as a cause of death, affecting over 5 million people and with more than 500,000 new cases diagnosed each year.1 The health care expenditures associated with heart failure were $26.7 billion in 2004 and are estimated to $33.2 billion in 2007. Although significant progress has been made in mechanical devices and pharmacological interventions, more than half of the patients with heart failure die within 5 years of initial diagnosis. Wide application of heart transplantation is severely hindered by the limited availability of donor organs. To this end, cardiac cell therapy may be an appealing alternative to current treatments for heart failure.

Recent investigations focusing on engineering cells and tissues to repair or regenerate damaged hearts in animal models and in clinical trials have yielded promising results. Considering the limited regenerative capacity of the heart muscle, renewable sources of cardiomyocytes are highly sought. Cells suitable for myocardial engineering should be nonimmunogenic, should be easy to expand to large quantities, and should differentiate into mature, fully functional cardiomyocytes capable of integrating to the host tissue. Adult progenitor cells (APCs) and embryonic stem cells (ESCs) have extensive proliferative potential and can adopt different cell fates, including that of heart cells. The recent advances in the fields of stem cell biology and heart tissue engineering have intensified efforts toward the development of regenerative cardiac therapies. In this article, we review findings pertaining to the cardiogenic potential of major APC populations and of ESCs (). We also discuss significant challenges in the way of realizing stem cellbased therapies aiming to reconstitute the normal function of heart.

Potential sources of stem/progenitor cells for cardiac repair. ESCs derived from the inner cell mass of a blastocyst can be manipulated ex vivo to differentiate toward heart cells. APCs residing in various tissues such as the BM and skeletal muscle may ...

Bone marrow (BM) is a heterogeneous tissue comprising of multiple cell types, including minute fractions of mesenchymal stem cells (MSCs; 0.0010.01% of total cells2) and hematopoietic stem cells (HSCs; 0.71.5cells/108 nucleated marrow cells3). The heterogeneity of BM makes challenging the identification of a subpopulation of cells capable of cardiogenesis, and studies of BM celltocardiac cell transdifferentiation should be examined through this prism.

The notion that BM-derived cells may contribute to the regeneration of the heart was first illustrated when dystrophic (mdx) female mice received BM cells from male wild-type mice.4 More than 2 months after the transplantation, tissues of the recipient mice were histologically examined for the presence of Y-chromosome+ donor cells. Besides the skeletal muscle, donor cells were identified in the cardiac region, suggesting that circulating BM cells contribute to the regeneration of cardiomyocytes.

Further supporting evidence was provided by Jackson et al.5 in studies using a side population (SP) of cells characterized by their intrinsic capacity to efflux Hoechst 33342 dye through the ATP-binding Bcrp1/ABCG2 transporter. The cells were isolated from the BM fraction of HSCs of Rosa26 mice constitutively expressing the -galactosidase reporter gene (LacZ). After SP cells were injected into mice with coronary occlusioninduced ischemia, cells coexpressing LacZ and cardiac -actinin were identified around the infarct region with a frequency of 0.02%. Endothelial engraftment was more prevalent (3.3%). The observed improvement in myocardial function may thus be attributed to the potential of BM cells to give rise to a rather endothelial progeny. This may be a parallel to cardiovascular progenitors from differentiating ESCs giving rise to cardiomyocytes, and endothelial and vascular smooth muscle lineages.6,7

Orlic et al.8 also reported the regeneration of infarcted myocardium after transplantation of lineage-negative (LIN)/C-KIT+ BM cells from transgenic mice constitutively expressing enhanced green fluorescent protein (eGFP). Cells were injected in the contracting wall close to the infarct area. Nine days after transplantation, an impressive 68% of the infarct was occupied by newly formed myocardium with eGFP+ cells displaying cardiomyocyte markers such as troponin, MEF2, NKX2.5, cardiac myosin, GATA-4, and -sarcomeric actin. Similar outcomes were reported by the same group9 when mouse C-KIT+ (but not screened for LIN) BM cells were transplanted.

Although these findings led to the conclusion that BM cells can repopulate a damaged heart, work by other investigators has casted doubt on this assertion. Balsam et al.10 noted that mice with infarcts receiving BM LIN/C-KIT+, C-KIT-enriched or THY1.1low/LIN/stem cell antigen-1 (SCA-1+) cells exhibited improved ventricular function. However, donor cells expressed granulocyte but not heart cell markers 1 month after injection. In another study,11 HSCs carrying a nuclear-localized LacZ gene flanked by the cardiac -myosin heavy chain promoter were delivered into the periinfarct zone of mice 5h after coronary artery occlusion. One to 4 weeks later, LacZ+ cells were absent in heart tissue sections from 117 mice that received HSCs. Similarly, no eGFP+ cells were detected in the infarcted hearts of mice infused with BM cells constitutively expressing eGFP. Finally, Nygren et al.12 in similar transplantation experiments observed only blood cells (mainly leukocytes) originating from BM HSCs in the infarcted myocardium without evidence of transdifferentiation of donor cells to cardiomyocytes.

Continued here:
Stem Cells for Heart Cell Therapies - National Center for ...

Cardiac stem cells, which have the ability to differentiate (specialize) into mature heart cells and therefore could be used to repair damaged or diseased heart tissue, have garnered significant interest in the development of treatments for heart disease and cardiac defects. Cardiac stem cells can be derived from mature cardiomyocytes through the process of dedifferentiation, in which mature heart cells are stimulated to revert to a stem cell state. The stem cells can then be stimulated to redifferentiate into myocytes or endothelial cells. This approach enables millions of cardiac stem cells to be produced in the laboratory.

In 2009 a team of doctors at Cedars-Sinai Heart Institute in Los Angeles, California, reported the first attempted use of cardiac stem cell transplantation to repair damaged heart tissue. The team removed a small section of tissue from the heart of a patient who had suffered a heart attack, and the tissue was cultured in a laboratory. Cells that had been stimulated to dedifferentiate were then used to produce millions of cardiac stem cells, which were later reinfused directly into the heart of the patient through a catheter in a coronary artery. A similar approach was used in a subsequent clinical trial reported in 2011; this trial involved 14 patients suffering from heart failure who were scheduled to undergo cardiac bypass surgery. More than three months after treatment, there was slight but detectable improvement over cardiac bypass surgery alone in left ventricle ejection fraction (the percentage of the left ventricular volume of blood that is ejected from the heart with each ventricular contraction).

Stem cells derived from bone marrow, the collection of which is considerably less invasive than heart surgery, are also of interest in the development of regenerative heart therapies. The collection and reinfusion into the heart of bone marrow-derived stem cells within hours of a heart attack may limit the amount of damage incurred by the muscle.

There are many types of arterial diseases. Some are generalized and affect arteries throughout the body, though often there is variation in the degree they are affected. Others are localized. These diseases are frequently divided into those that result in arterial occlusion (blockage) and those that are nonocclusive in their manifestations.

Atherosclerosis, the most common form of arteriosclerosis, is a disease found in large and medium-sized arteries. It is characterized by the deposition of fatty substances, such as cholesterol, in the innermost layer of the artery (the intima). As the fat deposits become larger, inflammatory white blood cells called macrophages try to remove the lipid deposition from the wall of the artery. However, lipid-filled macrophages, called foam cells, grow increasingly inefficient at lipid removal and undergo cell death, accumulating at the site of lipid deposition. As these focal lipid deposits grow larger, they become known as atherosclerotic plaques and may be of variable distribution and thickness. Under most conditions the incorporation of cholesterol-rich lipoproteins is the predominant factor in determining whether or not plaques progressively develop. The endothelial injury that results (or that may occur independently) leads to the involvement of two cell types that circulate in the bloodplatelets and monocytes (a type of white blood cell). Platelets adhere to areas of endothelial injury and to themselves. They trap fibrinogen, a plasma protein, leading to the development of platelet-fibrinogen thrombi. Platelets deposit pro-inflammatory factors, called chemokines, on the vessel walls. Observations of infants and young children suggest that atherosclerosis can begin at an early age as streaks of fat deposition (fatty streaks).

Atherosclerotic lesions are frequently found in the aorta and in large aortic branches. They are also prevalent in the coronary arteries, where they cause coronary artery disease. The distribution of lesions is concentrated in points where arterial flow gives rise to abnormal shear stress or turbulence, such as at branch points in vessels. In general the distribution in most arteries tends to be closer to the origin of the vessel, with lesions found less frequently in more distal sites. Hemodynamic forces are particularly important in the system of coronary arteries, where there are unique pressure relationships. The flow of blood through the coronary system into the heart muscle takes place during the phase of ventricular relaxation (diastole) and virtually not at all during the phase of ventricular contraction (systole). During systole the external pressure on coronary arterioles is such that blood cannot flow forward. The external pressure exerted by the contracting myocardium on coronary arteries also influences the distribution of atheromatous obstructive lesions.

Excerpt from:
cardiovascular disease :: Cardiac stem cells | Britannica.com

Cardiac stem cells, which have the ability to differentiate (specialize) into mature heart cells and therefore could be used to repair damaged or diseased heart tissue, have garnered significant interest in the development of treatments for heart disease and cardiac defects. Cardiac stem cells can be derived from mature cardiomyocytes through the process of dedifferentiation, in which mature heart cells are stimulated to revert to a stem cell state. The stem cells can then be stimulated to redifferentiate into myocytes or endothelial cells. This approach enables millions of cardiac stem cells to be produced in the laboratory.

In 2009 a team of doctors at Cedars-Sinai Heart Institute in Los Angeles, California, reported the first attempted use of cardiac stem cell transplantation to repair damaged heart tissue. The team removed a small section of tissue from the heart of a patient who had suffered a heart attack, and the tissue was cultured in a laboratory. Cells that had been stimulated to dedifferentiate were then used to produce millions of cardiac stem cells, which were later reinfused directly into the heart of the patient through a catheter in a coronary artery. A similar approach was used in a subsequent clinical trial reported in 2011; this trial involved 14 patients suffering from heart failure who were scheduled to undergo cardiac bypass surgery. More than three months after treatment, there was slight but detectable improvement over cardiac bypass surgery alone in left ventricle ejection fraction (the percentage of the left ventricular volume of blood that is ejected from the heart with each ventricular contraction).

Stem cells derived from bone marrow, the collection of which is considerably less invasive than heart surgery, are also of interest in the development of regenerative heart therapies. The collection and reinfusion into the heart of bone marrow-derived stem cells within hours of a heart attack may limit the amount of damage incurred by the muscle.

There are many types of arterial diseases. Some are generalized and affect arteries throughout the body, though often there is variation in the degree they are affected. Others are localized. These diseases are frequently divided into those that result in arterial occlusion (blockage) and those that are nonocclusive in their manifestations.

Atherosclerosis, the most common form of arteriosclerosis, is a disease found in large and medium-sized arteries. It is characterized by the deposition of fatty substances, such as cholesterol, in the innermost layer of the artery (the intima). As the fat deposits become larger, inflammatory white blood cells called macrophages try to remove the lipid deposition from the wall of the artery. However, lipid-filled macrophages, called foam cells, grow increasingly inefficient at lipid removal and undergo cell death, accumulating at the site of lipid deposition. As these focal lipid deposits grow larger, they become known as atherosclerotic plaques and may be of variable distribution and thickness. Under most conditions the incorporation of cholesterol-rich lipoproteins is the predominant factor in determining whether or not plaques progressively develop. The endothelial injury that results (or that may occur independently) leads to the involvement of two cell types that circulate in the bloodplatelets and monocytes (a type of white blood cell). Platelets adhere to areas of endothelial injury and to themselves. They trap fibrinogen, a plasma protein, leading to the development of platelet-fibrinogen thrombi. Platelets deposit pro-inflammatory factors, called chemokines, on the vessel walls. Observations of infants and young children suggest that atherosclerosis can begin at an early age as streaks of fat deposition (fatty streaks).

Atherosclerotic lesions are frequently found in the aorta and in large aortic branches. They are also prevalent in the coronary arteries, where they cause coronary artery disease. The distribution of lesions is concentrated in points where arterial flow gives rise to abnormal shear stress or turbulence, such as at branch points in vessels. In general the distribution in most arteries tends to be closer to the origin of the vessel, with lesions found less frequently in more distal sites. Hemodynamic forces are particularly important in the system of coronary arteries, where there are unique pressure relationships. The flow of blood through the coronary system into the heart muscle takes place during the phase of ventricular relaxation (diastole) and virtually not at all during the phase of ventricular contraction (systole). During systole the external pressure on coronary arterioles is such that blood cannot flow forward. The external pressure exerted by the contracting myocardium on coronary arteries also influences the distribution of atheromatous obstructive lesions.

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cardiovascular disease :: Cardiac stem cells | Britannica.com

By the time Bill Beatty made it to the Emergency Department in Howard County, he was already several hours into a major heart attack. His physicians performed a series of emergency treatments that included an intra-aortic balloon pump, but the 57-year-old engineers blood pressure remained dangerously low. The cardiologist called for a helicopter to transfer him to Johns Hopkins.

It was fortuitous timing: Beatty was an ideal candidate for a clinical trial and soon received an infusion of stem cells derived from his own heart tissue, making him the second patient in the world to undergo the procedure.

Of all the attempts to harness the promise of stem cell therapy, few have garnered more hope than the bid to repair damaged hearts. Previous trials with other stem cells have shown conflicting results. But this new trial, conducted jointly with cardiologist Eduardo Marbn at Cedars-Sinai Medical Center in Los Angeles, is the first time stem cells come from the patients own heart.

Cardiologist Jeffrey Brinker, M.D., a member of the Hopkins team, thinks the new protocol could be a game-changer. That's based partly on recent animal studies in which scientists at both institutions isolated stem cells from the injured animals hearts and infused them back into the hearts of those same animals. The stem cells formed new heart muscle and blood vessel cells. In fact, says Brinker, the new cells have a pre-determined cardiac fate. Even in the culture dish, he says, theyre a beating mass of cells.

Whats more, according to Gary Gerstenblith, M.D., J.D., the animals in these studies showed a significant decrease in relative infarct size, shrinking by about 25 percent. Based on those and earlier findings, investigators were cleared by the FDA and Hopkins Institutional Review Board to move forward with a human trial.

In Beattys case, Hopkins heart failure chief Stuart Russell, M.D., extracted a small sample of heart tissue and shipped it to Cedars Sinai, where stem cells were isolated, cultured and expanded to large numbers. Hopkins cardiologist Peter Johnston, M.D., says cardiac tissue is robust in its ability to generate stem cells, typically yielding several million transplantable cells within two months.

When ready, the cells were returned to Baltimore and infused back into Beatty through a balloon catheter placed in his damaged artery, ensuring target-specific delivery. Then the watching and waiting began. For the Hopkins team, Beattys infarct size will be tracked by imaging chief Joao Lima, M.D., M.B.A.,and his associates using MRI scans.

Now back home and still struggling with episodes of compromised stamina and shortness of breath, Beatty says his Hopkins cardiologists were fairly cautious in their prognosis, but hell be happy for any improvement.

Nurse coordinator Elayne Breton says Beatty is scheduled for follow-up visits at six months and 12 months, when they hope to find an improvement in his hearts function. But at least one member of the Hopkins team was willing acknowledge a certain optimism. The excitement here, says Brinker, is huge.

The trial is expected to be completed within one to two years.

Originally posted here:
Stem Cell Research at Johns Hopkins Medicine: Repairing ...

Tsai et al./Stem Cell Reports 2015

Weill Cornell investigators have discovered how to generate large numbers of rare cells in the network that pushes the heart's chambers to consistently contract. In this image, investigators stained these cells, generated from embryonic stem cells, to reveal cell-specific genes (green and red, indicated by arrows). The blue represents stained cell nuclei.

For the first time, scientists can efficiently generate large numbers of rare cells in the network that pushes the heart's chambers to consistently contract. The technique, published May 28 in Stem Cell Reports, could be a first step toward using a person's own cells to repair an irregular heartbeat known as cardiac arrhythmia.

This study, while done using mouse cells, will now allow us to develop human heart cells and test their function in repairing damaged hearts, said the study's senior author, Dr. Todd Evans, vice chair for research and the Peter I. Pressman Professor in the Department of Surgery at Weill Cornell Medical College.

The human heart beats billions of times during a lifetime, so it's not surprising that development of irregular heartbeats can lead to a variety of cardiac diseases, Evans says. But treatments for these disorders are costly, and often ineffective.

The government pays more than $3 billion each year for cardiac arrhythmia-related diseases. Despite this enormous expense, the treatments we have available are inadequate, Evans said. For example, artificial pacemakers are often used, but these can fail, and are particularly challenging therapies for children.

One solution is to coax a patient's own cells to generate the specific kinds of cells in the cardiac conduction system (CCS) that maintain a regular heartbeat.

We can imagine someday using these cells, for example, to create patches that can replace defective conduction fibers. Of course this is still a long way off, as we would need to study how to coax them into integrating properly with the rest of the CCS, Evans said. But previously, we did not even have the capacity to generate the cells, and now we can do so in a manner that is scalable, so that such preclinical research is now feasible.

Evans worked with Dr. Shuibing Chen, an expert in stem cell and chemical biology, and Dr. Su-Yi Tsai, a postdoctoral fellow and the study's lead investigator. Other key contributors were from the laboratory of Dr. Glenn Fishman, who specializes in cardiac physiology at New York University.

Their first goal was to increase the efficiency of coaxing mouse embryonic stem cells to become CCS cells. They created mouse stem cells that can express a CCS marker gene that can be quantified. This allows them to measure how many embryonic cells morph into CCS cells.

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Stem cell technology could lead to ailing heart mending ...

Charles A. Goldthwaite, Jr., Ph.D.

Cardiovascular disease (CVD), which includes hypertension, coronary heart disease (CHD), stroke, and congestive heart failure (CHF), has ranked as the number one cause of death in the United States every year since 1900 except 1918, when the nation struggled with an influenza epidemic.1 In 2002, CVD claimed roughly as many lives as cancer, chronic lower respiratory diseases, accidents, diabetes mellitus, influenza, and pneumonia combined. According to data from the 19992002 National Health and Nutrition Examination Survey (NHANES), CVD caused approximately 1.4 million deaths (38.0 percent of all deaths) in the U.S. in 2002. Nearly 2600 Americans die of CVD each day, roughly one death every 34 seconds. Moreover, within a year of diagnosis, one in five patients with CHF will die. CVD also creates a growing economic burden; the total health care cost of CVD in 2005 was estimated at $393.5 billion dollars.

Given the aging of the U.S. population and the relatively dramatic recent increases in the prevalence of cardiovascular risk factors such as obesity and type 2 diabetes,2,3 CVD will continue to be a significant health concern well into the 21st century. However, improvements in the acute treatment of heart attacks and an increasing arsenal of drugs have facilitated survival. In the U.S. alone, an estimated 7.1 million people have survived a heart attack, while 4.9 million live with CHF.1 These trends suggest an unmet need for therapies to regenerate or repair damaged cardiac tissue.

Ischemic heart failure occurs when cardiac tissue is deprived of oxygen. When the ischemic insult is severe enough to cause the loss of critical amounts of cardiac muscle cells (cardiomyocytes), this loss initiates a cascade of detrimental events, including formation of a non-contractile scar, ventricular wall thinning (see Figure 6.1), an overload of blood flow and pressure, ventricular remodeling (the overstretching of viable cardiac cells to sustain cardiac output), heart failure, and eventual death.4 Restoring damaged heart muscle tissue, through repair or regeneration, therefore represents a fundamental mechanistic strategy to treat heart failure. However, endogenous repair mechanisms, including the proliferation of cardiomyocytes under conditions of severe blood vessel stress or vessel formation and tissue generation via the migration of bone-marrow-derived stem cells to the site of damage, are in themselves insufficient to restore lost heart muscle tissue (myocardium) or cardiac function.5 Current pharmacologic interventions for heart disease, including beta-blockers, diuretics, and angiotensin-converting enzyme (ACE) inhibitors, and surgical treatment options, such as changing the shape of the left ventricle and implanting assistive devices such as pacemakers or defibrillators, do not restore function to damaged tissue. Moreover, while implantation of mechanical ventricular assist devices can provide long-term improvement in heart function, complications such as infection and blood clots remain problematic.6 Although heart transplantation offers a viable option to replace damaged myocardium in selected individuals, organ availability and transplant rejection complications limit the widespread practical use of this approach.

Figure 6.1. Normal vs. Infarcted Heart. The left ventricle has a thick muscular wall, shown in cross-section in A. After a myocardial infarction (heart attack), heart muscle cells in the left ventricle are deprived of oxygen and die (B), eventually causing the ventricular wall to become thinner (C).

2007 Terese Winslow

The difficulty in regenerating damaged myocardial tissue has led researchers to explore the application of embryonic and adult-derived stem cells for cardiac repair. A number of stem cell types, including embryonic stem (ES) cells, cardiac stem cells that naturally reside within the heart, myoblasts (muscle stem cells), adult bone marrow-derived cells, mesenchymal cells (bone marrow-derived cells that give rise to tissues such as muscle, bone, tendons, ligaments, and adipose tissue), endothelial progenitor cells (cells that give rise to the endothelium, the interior lining of blood vessels), and umbilical cord blood cells, have been investigated to varying extents as possible sources for regenerating damaged myocardium. All have been tested in mouse or rat models, and some have been tested in large animal models such as pigs. Preliminary clinical data for many of these cell types have also been gathered in selected patient populations.

However, clinical trials to date using stem cells to repair damaged cardiac tissue vary in terms of the condition being treated, the method of cell delivery, and the primary outcome measured by the study, thus hampering direct comparisons between trials.7 Some patients who have received stem cells for myocardial repair have reduced cardiac blood flow (myocardial ischemia), while others have more pronounced congestive heart failure and still others are recovering from heart attacks. In some cases, the patient's underlying condition influences the way that the stem cells are delivered to his/her heart (see the section, quot;Methods of Cell Deliveryquot; for details). Even among patients undergoing comparable procedures, the clinical study design can affect the reporting of results. Some studies have focused on safety issues and adverse effects of the transplantation procedures; others have assessed improvements in ventricular function or the delivery of arterial blood. Furthermore, no published trial has directly compared two or more stem cell types, and the transplanted cells may be autologous (i.e., derived from the person on whom they are used) or allogeneic (i.e., originating from another person) in origin. Finally, most of these trials use unlabeled cells, making it difficult for investigators to follow the cells' course through the body after transplantation (see the section quot;Considerations for Using These Stem Cells in the Clinical Settingquot; at the end of this article for more details).

Despite the relative infancy of this field, initial results from the application of stem cells to restore cardiac function have been promising. This article will review the research supporting each of the aforementioned cell types as potential source materials for myocardial regeneration and will conclude with a discussion of general issues that relate to their clinical application.

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6. Mending a Broken Heart: Stem Cells and Cardiac Repair ...

Rationale: Autologous bone marrowderived or cardiac-derived stem cell therapy for heart disease has demonstrated safety and efficacy in clinical trials, but functional improvements have been limited. Finding the optimal stem cell type best suited for cardiac regeneration is the key toward improving clinical outcomes.

Objective: To determine the mechanism by which novel bone-derived stem cells support the injured heart.

Methods and Results: Cortical bonederived stem cells (CBSCs) and cardiac-derived stem cells were isolated from enhanced green fluorescent protein (EGFP+) transgenic mice and were shown to express c-kit and Sca-1 as well as 8 paracrine factors involved in cardioprotection, angiogenesis, and stem cell function. Wild-type C57BL/6 mice underwent sham operation (n=21) or myocardial infarction with injection of CBSCs (n=67), cardiac-derived stem cells (n=36), or saline (n=60). Cardiac function was monitored using echocardiography. Only 2/8 paracrine factors were detected in EGFP+ CBSCs in vivo (basic fibroblast growth factor and vascular endothelial growth factor), and this expression was associated with increased neovascularization of the infarct border zone. CBSC therapy improved survival, cardiac function, regional strain, attenuated remodeling, and decreased infarct size relative to cardiac-derived stem cells or saline-treated myocardial infarction controls. By 6 weeks, EGFP+ cardiomyocytes, vascular smooth muscle, and endothelial cells could be identified in CBSC-treated, but not in cardiac-derived stem cellstreated, animals. EGFP+ CBSC-derived isolated myocytes were smaller and more frequently mononucleated, but were functionally indistinguishable from EGFP myocytes.

Conclusions: CBSCs improve survival, cardiac function, and attenuate remodeling through the following 2 mechanisms: (1) secretion of proangiogenic factors that stimulate endogenous neovascularization, and (2) differentiation into functional adult myocytes and vascular cells.

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Bone-Derived Stem Cells Repair the Heart After Myocardial ...

Clara's Story

Clara had a severe heart attack in 2004. Before contacting us she had received adult stem cells from a company in Thailand - a process requiring at least a one week stay.

When she contacted Stemaid, she had just had an echocardiogram showing that her overall left ventricular ejection fraction was estimated to be 30 to 35%. She opted to receive one injection of 5 million Embryonic Stem Cells by Stemaid in November 2010. She arrived at 1pm and was done by 3pm the same day.

We received the following email from her in April 2011: I had an EKO last week and rate is 44%, up from the 33/35% it was before I received Stemaid's stem cells! . Are the stem cells still available and still as good?

The heart contains a small amount of stem cells, the cardiac stem cells, that are produced when there is a need for production of more heart cells or for an active replacement of damaged ones. These cardiac cells are produced in high quantity for about one week following an infarction, actively repairing the damaged areas of the heart.

However this high production stops after a week and the repair stops as well.

Initial studies showed that by introducing embryonic stem cells, the heart starts to repair again within minutes of their injection. More recent studies showed that the injection of embryonic stem cells actually triggers the production of cardiac stem cells for one week. Another week of active repair is offered each time that one receives embryonic stem cells.

If you have suffered from an infarction, we suggest a minimum of 3 injections of esc over the course of 3 weeks to get significant repair.

Some of the patients who have received Stemaid Embryonic Stem-Cells have agreed to be mentioned on our website so that we may illustrate the benefits of them.

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Heart Disease - Stemaid : Embryonic Stem-cells

Stem cells: When will they heal the heart?

Its been 15 years since a University of Wisconsin-Madison researcher isolated embryonic stem cells the do-anything cells that appear in early development. Its been six years since adult human cells were transformed into the related induced pluripotent stem cells.

ENLARGE

Some day, stem cell therapy could restore cells, save hearts, and avoid the need for some heart transplants, such as this one. This heart is ready for its new home.

And yet the early hope to grow spare parts turning stem cells into specialized cells for repairing a failing brain, pancreas or heart, remains mostly promise rather than reality.

Researchers have since found how to transform stem cells into a wide variety of body cells, including heart muscle cells, or cardiomyocytes. But the holy Grail tissue supplementation or replacement remains tantalizingly out of reach.

Last week, Why Files attended a symposium on treating cardiovascular disease with stem cells, at the BioPharmaceutical Technology Center Institute near Madison, Wis. We found the picture unexpectedly complicated: as multiple kinds of stem cells are grown and delivered in a bewildering variety of ways to treat a catalog of conditions.

So far, stem cells have not been approved to treat any heart disease in the United States.

Still, the need remains clear. Disorders of the heart and blood vessels, which deliver oxygen and nutrients to the body, continue to kill. Today, one of every 2.6 Americans will die of some cause related to their heart, writes Columbia University Medical Center.

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Stem cell therapy : When will it help the heart? | The Why ...

Heart attacks and congestive heart failure remain among the Nation's most prominent health challenges despite many breakthroughs in cardiovascular medicine. In fact, despite successful approaches to prevent or limit cardiovascular disease, the restoration of function to the damaged heart remains a formidable challenge. Recent research is providing early evidence that adult and embryonic stem cells may be able to replace damaged heart muscle cells and establish new blood vessels to supply them. Discussed here are some of the recent discoveries that feature stem cell replacement and muscle regeneration strategies for repairing the damaged heart.

For those suffering from common, but deadly, heart diseases, stem cell biology represents a new medical frontier. Researchers are working toward using stem cells to replace damaged heart cells and literally restore cardiac function.

Today in the United States, congestive heart failurethe ineffective pumping of the heart caused by the loss or dysfunction of heart muscle cellsafflicts 4.8 million people, with 400,000 new cases each year. One of the major contributors to the development of this condition is a heart attack, known medically as a myocardial infarction, which occurs in nearly 1.1 million Americans each year. It is easy to recognize that impairments of the heart and circulatory system represent a major cause of death and disability in the United States [5].

What leads to these devastating effects? The destruction of heart muscle cells, known as cardiomyocytes, can be the result of hypertension, chronic insufficiency in the blood supply to the heart muscle caused by coronary artery disease, or a heart attack, the sudden closing of a blood vessel supplying oxygen to the heart. Despite advances in surgical procedures, mechanical assistance devices, drug therapy, and organ transplantation, more than half of patients with congestive heart failure die within five years of initial diagnosis. Research has shown that therapies such as clot-busting medications can reestablish blood flow to the damaged regions of the heart and limit the death of cardiomyocytes. Researchers are now exploring ways to save additional lives by using replacement cells for dead or impaired cells so that the weakened heart muscle can regain its pumping power.

How might stem cells play a part in repairing the heart? To answer this question, researchers are building their knowledge base about how stem cells are directed to become specialized cells. One important type of cell that can be developed is the cardiomyocyte, the heart muscle cell that contracts to eject the blood out of the heart's main pumping chamber (the ventricle). Two other cell types are important to a properly functioning heart are the vascular endothelial cell, which forms the inner lining of new blood vessels, and the smooth muscle cell, which forms the wall of blood vessels. The heart has a large demand for blood flow, and these specialized cells are important for developing a new network of arteries to bring nutrients and oxygen to the cardiomyocytes after a heart has been damaged. The potential capability of both embryonic and adult stem cells to develop into these cells types in the damaged heart is now being explored as part of a strategy to restore heart function to people who have had heart attacks or have congestive heart failure. It is important that work with stem cells is not confused with recent reports that human cardiac myocytes may undergo cell division after myocardial infarction [1]. This work suggests that injured heart cells can shift from a quiescent state into active cell division. This is not different from the ability of a host of other cells in the body that begin to divide after injury. There is still no evidence that there are true stem cells in the heart which can proliferate and differentiate.

Researchers now know that under highly specific growth conditions in laboratory culture dishes, stem cells can be coaxed into developing as new cardiomyocytes and vascular endothelial cells. Scientists are interested in exploiting this ability to provide replacement tissue for the damaged heart. This approach has immense advantages over heart transplant, particularly in light of the paucity of donor hearts available to meet current transplantation needs.

What is the evidence that such an approach to restoring cardiac function might work? In the research laboratory, investigators often use a mouse or rat model of a heart attack to study new therapies (see Figure 9.1. Rodent Model of Myocardial Infarction). To create a heart attack in a mouse or rat, a ligature is placed around a major blood vessel serving the heart muscle, thereby depriving the cardiomyocytes of their oxygen and nutrient supplies. During the past year, researchers using such models have made several key discoveries that kindled interest in the application of adult stem cells to heart muscle repair in animal models of heart disease.

Figure 9.1. Rodent Model of Myocardial Infarction.

( 2001 Terese Winslow, Lydia Kibiuk)

Recently, Orlic and colleagues [9] reported on an experimental application of hematopoietic stem cells for the regeneration of the tissues in the heart. In this study, a heart attack was induced in mice by tying off a major blood vessel, the left main coronary artery. Through the identification of unique cellular surface markers, the investigators then isolated a select group of adult primitive bone marrow cells with a high capacity to develop into cells of multiple types. When injected into the damaged wall of the ventricle, these cells led to the formation of new cardiomyocytes, vascular endothelium, and smooth muscle cells, thus generating de novo myocardium, including coronary arteries, arterioles, and capillaries. The newly formed myocardium occupied 68 percent of the damaged portion of the ventricle nine days after the bone marrow cells were transplanted, in effect replacing the dead myocardium with living, functioning tissue. The researchers found that mice that received the transplanted cells survived in greater numbers than mice with heart attacks that did not receive the mouse stem cells. Follow-up experiments are now being conducted to extend the posttransplantation analysis time to determine the longer-range effects of such therapy [8]. The partial repair of the damaged heart muscle suggests that the transplanted mouse hematopoietic stem cells responded to signals in the environment near the injured myocardium. The
cells migrated to the damaged region of the ventricle, where they multiplied and became "specialized" cells that appeared to be cardiomyocytes.

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9. Can Stem Cells Repair a Damaged Heart? [Stem Cell ...

Could this experimental treatment reverse damage caused by a heart attack?

The heart muscle relies on a steady flow of oxygen-rich blood to nourish it and keep it pumping. During a heart attack, that blood flow is interrupted by a blockage in an artery. Without blood, the area of heart fed by the affected artery begins to die and scar tissue forms in the area. Over time, this damage can lead to heart failure, especially when one heart attack comes after another.

Though the heart is a tough organ, the damaged portions become unable to pump blood as efficiently as they once could. People who have had a heart attack therefore may face a lifetime of maintenance therapymedications and other treatments aimed at preventing another heart attack and helping the heart work more efficiently.

A new treatment using stem cellswhich have the potential to grow into a variety of heart cell typescould potentially repair and regenerate damaged heart tissue. In a study published last February in The Lancet, researchers treated 17 heart attack patients with an infusion of stem cells taken from their own hearts. A year after the procedure, the amount of scar tissue had shrunk by about 50%.

These results sound dramatic, but are they an indication that we're getting close to perfecting this therapy? "This is a field where, depending on which investigator you ask, you can get incredibly different answers," says Dr. Richard Lee, professor of medicine at Harvard Medical School and a leading expert on stem cell therapy.

"The field is young. Some studies show only modest or no improvement in heart function, but others have shown dramatically improved function," he says. "We're waiting to see if other doctors can also achieve really good results in other patients."

Studies are producing such varied outcomes in part because researchers are taking different approaches to harvesting and using stem cells. Some stem cells are taken from the bone marrow of donors, others from the patient's own heart. It's not clear which approach is the most promising.

Several different types of approaches are being used to repair damaged heart muscle with stem cells. The stem cells, which are often taken from bone marrow, may be inserted into the heart using a catheter. Once in place, stem cells help regenerate damaged heart tissue.

Like any other therapy, injecting stem cells into the heart can fail or cause side effects. If the stem cells are taken from an unrelated donor, the body's immune system may reject them. And if the injected cells can't communicate with the heart's finely tuned electrical system, they may produce dangerous heart rhythms (arrhythmias). So far, side effects haven't been a major issue, though, and that has encouraged investigators to push onward.

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Repairing the heart with stem cells - Harvard Health

Welcome

The Stem Cell Center Texas Heart Institute is dedicated to the study of adult stem cells and their role in treating diseases of the heart and the circulatory system. Through numerous clinical and preclinical studies, we have come to realize the potential of stem cells to help patients suffering from cardiovascular disease.We are actively enrolling patients in studies using stem cells for the treatment of heart failure, heart attacks, and peripheral vascular disease.

Whether you are a patient looking for information regarding our research, or a doctor hoping to learn more about stem cell therapy, we welcome you to the Stem Cell Center. Please visit our Clinical Trials page for more information about our current trials.

Emerson C. Perin, MD, PhD, FACC Director, Clinical Research for Cardiovascular Medicine Medical Director, Stem Cell Center McNair Scholar

You may contact us at:

E-mail: stemcell@texasheart.org Toll free: 1-866-924-STEM (7836) Phone: 832-355-9405 Fax: 832-355-9440

We are a network of physicians, scientists, and support staff dedicatedto studying stem cell therapy for treating heart disease. Thegoals of the Network are to complete research studies that will potentially lead to more effective treatments for patients with cardiovasculardisease, and to share knowledge quickly with the healthcare community.

Websitein Spanish (En espaol)

Follow this link:
The Stem Cell Center at Texas Heart Institute

For millions of people around the world, who suffer from various diseases, research in stem cells offers a ray of hope. Scientists of the city-based Indian Institute of Science have used stem cells of a mouse to culture cardiac cells.

Explaining the research, Polani B. Seshagiri said their research over the past seven years has helped develop cardiac cells that function and beat in rhythms identical to the original cell.

Speaking on Stem Cell Awareness Day recently, Prof. Seshagiri said stem cells had several advantages and could cure human disorders and diseases, which could not be cured by conventional approaches. However, he warned that there was a need to be aware of the limitations of stem cells.

Sudarshan Ballal, Medical Director, Manipal Health Enterprise, said stem cells had enormous potential as they never die and could be converted into any cell. Stem cells can be converted into organs and maybe years later, organs can be cultivated in labs through stem cell, he said. Elaborating further, he said a stem cell could be compared to a bicycle, which could turn into car, motorbike and spaceship based on the environment and conditions.

Nazeer Ahmed, Deputy Drug Controller of Karnataka, said they were in the process of chalking out regulations for stem cells as there were currently no rules to regulate stem cell research and therapy.

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Scientists develop cardiac cells using stem cells

Dr. Gabriele DUva is finishing up his postdoctoral research at the Weizmann Institute. Here is his account of three years of highly successful research on regenerating heart cells after injury. Among other things, it is the story of the way that different ideas from vastly different research areas can, over the dinner table or in casual conversation, provide the inspiration for outstanding research:

Three years ago, when I joined the lab of Prof. Eldad Tzahor, the emerging field of cardiac regeneration was totally obscure to me. My scientific track at that time was mainly focused on normal and cancer stem cells: cells that build our bodies during development and adulthood. The deregulation of these cells can lead to cancer. I have to admit that I didnt know even the shape of a cardiac cell when my postdoc journey started

Eldads lab was also switching fields well, not drastically, like me, but still it was a transition from a basic research on the development of the heart to the challenge of heart regeneration during adult life.

Two neonatal cardiomyocytes (staining in red) undergoing cell division after treatment with NRG1

In contrast to most tissues in our body, which renew themselves throughout life using our pools of stem cells, the renewal of heart cells in adulthood is extremely low; it almost doesnt exist. Just to give an approximate picture of renewal and regeneration processes: Every day we produce billions of new blood cells that completely replace the old ones in a few months. In contrast, heart cells renewal is so low that, many cardiac cells remain with us for our entire life, from birth to death! Consequently, heart injuries cannot be truly repaired, leading to (often lethal) cardiovascular diseases. This might appear somewhat nonsensical, since the heart is our most vital organ: No (heart) beat no life.

Hence a challenge for many scientists is to understand how to induce heart regeneration Scientists have been trying different strategies, for example, the injection of stem cells. We decided to adopt a different strategy one that mimics the natural regenerative process of healing the heart in such regenerative organisms as amphibians and fish, and even newly-born mice. In all these cases the regeneration of the heart involves the proliferation of heart muscle cells called cardiomyocytes. Therefore the challenge before us was: How can we push cardiomyocytes to divide?

We adopted a team strategy. Cancer turned out to be a somewhat useful model for a strategy. After all, the hallmark of this disease is continuous self-renewal and cell proliferation. Starting from this thought, Prof. Yossi Yarden, a leading expert in the cancer field, suggested: Why dont you try an oncogene, such as ERBB2, whose deregulation can lead to uncontrolled cellular growth and tumour development? The idea was that cardiomyocytes could be pushed into a proliferative state by this cancer-promoting agent. To Eldad, this was a nice life circle closing, since Eldad, when he was a PhD student in Yossis lab, focused exactly on the ERBB2 mechanism of action in cancer progression. I must admit, the idea sounded very intriguing and I really liked it.

Eldad, as a developmental biologist, had a different approach. Based on his field of expertise, his tactic was to apply proliferative (and regenerative) strategies learned from the embryos, when heart cells normally proliferate to form a functional organ. It turned out that a key player in driving embryonic heart growth is again ERBB2!

Read more here:
Guest post: Dr. Gabriele DUva: How to Grow New Heart Cells [The Weizmann Wave]

Theres been a lot of talk lately about how spider silk is this crazy wonder material that may soon find its way into everything from electronics to ultra-strong fabrics. Now, theres another reason to be excited about spider silk: doctors might one day use the stuff to grow you a new heart.

Growing new organs and tissues outside the body is the bleeding edge of biomedical research. Just imagine: if doctors could grow replacement hearts or kidneys from a patients own stem cells, that patient would no longer have to face the agonizing prospect of waiting to find a suitable donor. The risk of organ rejection would become nil. But theres a lot of R&D to be done before we get there. One initial challenge has been finding a scaffold material to grow organ tissues onsomething thats non-toxic, will not impede cell growth, and will not, itself, be rejected by the body. That, it turns out, is a pretty tall order.

But, as described in a study published recently in PLOS ONE, genetically engineered fibers of spidrointhe protein that builds cobweb strandsmight just fit the bill when it comes to human heart tissue. Spidroin fibers have already proven themselves a useful substrate for growing tendons and cartilages. Researchers at the Moscow Institute for Physics and Technology decided to see whether spidroin grown in the lab via genetically modified yeast cells can also be used to grow cardiomycetes, the cells that form heart tissue.

Heart tissue cells grown on a matrix and stained with fluorescent markers via Alexander Teplenin et al. / PLOS ONE

For their experiments, the researchers seeded a spidroin fiber matrix with neonatal rat cardiomycetes. Within 3 to 5 days, a layer of cardiac cells had formed. Follow-up tests determined that this tissue was able to contract synchronously and conduct electrical impulses, just like normal heart tissue should

Itll probably be some years yet before were growing full human hearts on any sort of artificial scaffold, but its exciting to see that progress is being made toward that goal. If the idea of an artificial heart thats stitched together with spider webs sounds a bit creepy, know this: those fibers are five times stronger than steel and twice as elastic as nylon. If anything, it sounds like an upgrade.

Read the full open-access scientific paper at PLOS ONE.

Top image via Shutterstock

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In The Future, Spider Silk May Help Grow Your Replacement Heart

BENGALURU: The day may not be far when organs can be cultured in labs using stem cells. Making a headway in that direction are Indian Institute of Science scientists who have cultured the cardiac cells of a mouse using stem cells.

Stem cells are capable of turning into specific types of cells. "We researched on developing the cardiac cell of a mouse for over seven years. The challenge now is to study how stem cells can be used to produce different organs," said Polani B Seshagiri on the occasion of Stem Cell Awareness Day on Friday. The professor of IISc's department of molecular reproduction, development and genetics headed the study.

Polani who has been researching on stem cells for three decades, said these cells offer many advantages in curing human disorders which otherwise aren't curable using conventional medical approaches. "However, it's extremely important to be aware of their limitations too," he added.

Stay updated on the go with Times of India News App. Click here to download it for your device.

Originally posted here:
Mouse's cardiac cells grown in lab

CIRM funds many projects seeking to better understand heart disease and to translate those discoveries into new therapies.

If you want to learn more about CIRM funding decisions or make a comment directly to our board, join us at a public meeting. You can find agendas for upcoming public meetings on our meetings page.

Find Out More: Stem Cell FAQ | Stem Cell Videos | What We Fund

Find clinical trials: CIRM does not track stem cell clinical trials. If you or a family member is interested in participating in a clinical trial, please visit clinicaltrials.gov to find a trial near you.

Heart disease strikes in many forms, but collectively it causes one third of all deaths in the U.S. Many forms of heart disease have a common resultcardiomyopathy. While this is commonly called congestive heart failure (CHF), it is really just the heart becoming less efficient due to any number of causes, but the most common is loss of functioning heart muscle due to the damage caused by a heart attack. An estimated 4.8 million Americans have CHF, with 400,000 new cases diagnosed each year. Half die within five years.

Numerous clinical trials are underway testing a type of stem cell found in borne marrow, called mesenchymal stem cells or MSCs, to see if they are effective in treating the form of CHF that follows a heart attack. While those trials have shown some small improvements in patients the researchers have not found that the MSCs are creating replacement heart muscle. They think the improvements may be due to the MSCs creating new blood vessels that then help make the existing heart muscle healthier, or in other ways strengthening the existing tissue.

Californias stem cell agency has numerous awards looking into heart disease (the full list is below). Most of these involve looking for ways to create stem cells that can replace the damaged heart muscle, restoring the hearts ability to efficiently pump blood around the body. Some researchers are looking to go beyond transplanting cells into the heart and are instead exploring the use of tissue engineering technologies, such as building artificial scaffolds in the lab and loading them with stem cells that, when placed in the heart, may stimulate the recovery of the muscle.

Other CIRM-funded researchers are working in the laboratory, looking at stem cells from heart disease patients to better understand the disease and even using those models to discover and test new drugs to see if they are effective in treating heart disease. Other researchers are trying to make a type of specialized heart cell called a pacemaker cell, which helps keep a proper rhythm to the hearts beat.

We also fund projects that are trying to take promising therapies out of the laboratory and closer to being tested in people. These Disease Team Awards encourage the creation of teams that have both the scientific knowledge and business skills needed to produce therapies that can get approval from the Food and Drug Administration (FDA) to be tested in people. In some cases, these awards also fund the early phase clinical trials to show that they are safe to use and, in some cases, show some signs of being effective.

This team developed a way to isolate some heart-specific stem cells that are found in adult heart muscle. They use clumps of cells called Cardiospheres to reduce scarring caused by heart attacks. Initially they used cells obtained from the patients own heart but they later developed methods to obtain the cells they need from donor organs, which allows the procedure to become an off-the-shelf-therapy, meaning it can be available when and where the patient needs it rather than having to create it new each time. The company, working with the Cedars-Sinai team, received FDA approval to begin a clinical trial in June 2012.

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Heart Disease Fact Sheet | California's Stem Cell Agency

CardioCel has been initially well received with surgeons in Australia and overseas. Photo: Geoff Fisher

For 10 years researchers at Admedus worked day and night trying to work out how to improve soft tissue repair in the human body.

And with the vital help of CSIRO they have been to develop CardioCel, a life-saving heart patch for the repair and reconstruction of cardiovascular defects.

According to the Children's Heart Foundation, congenital heart disease occurs in one out of 100 births and in at least half of those cases surgery is required and a patch is needed. They state it is the leading cause of birth defect related deaths.

Research undertaken with CSIRO investigated new, potentially ground-breaking applications for CardioCel. The research focused on using stem cells. It found the heart patch has the potential to deliver stem cells and help tissue heal better than other existing products, when used for cardiac repair.

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Derived from animal tissue, the CardioCel patch is engineered over 14 days.

"The first unique feature of this product is that it doesn't calcify in young patients," Professor Leon Neethling, Admedus technical director and heart researcher says.

The flexible patch works like human tissue to cover holes in the heart thereby eliminating the need for repeat surgery.

"In the cardiac repair field it has long been recognised that strong, flexible, biocompatible and calcification-resistant tissue scaffolds would be ideal tissues for repair of heart defects," Admedus' chief operating officer Dr Julian Chick, says.

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Local innovation repairs holes in the heart

Newport Beach, California (PRWEB) March 31, 2015

Newport Beach based charity Coalition Duchenne has launched an interview series titled Making a Difference in Duchenne on its Youtube channel (https://www.youtube.com/user/CoalitionDuchenne) focused on individuals making a difference in Duchenne muscular dystrophy research, care, awareness, and education.

The first interview features Dr. Eduardo Marbn MD, PhD, director of the Cedars-Sinai Heart Institute in Los Angeles, talking about cardiac derived stem cells. Dr. Marbn was featured in a November 2011 Economist article Repairing Broken Hearts, read by Coalition Duchenne founder and executive director Catherine Jayasuriya. She lobbied for a focus on Duchenne because cardiac scarring severely compromises the life span of those with the disease. Coalition Duchenne funded successful research applying Marbns stem cell technology to Duchenne. The approach has been clinically proven to mitigate scarring cause by heart attacks. In Marbns therapy, human heart tissue is used to grow specialized heart stem cells, which are injected back into the patients heart.

We need to focus on changing the course of the disease. We lose many young men to cardiac issues. We hope that working with cardiac stem cells is one way we will eventually change that outcome, said Jayasuriya.

The second interview in the Making a Difference in Duchenne series features actor Cody Saintgnue, who plays Brett Talbot in MTVs Teen Wolf. Saintgnue has a unique relationship with Duchenne. He played a young man with muscular dystrophy in his break out role on House MD in 2009. Saintgnue talks about his experience learning to mimic the physicality of a young man with Duchenne, as well as the inspiration he draws from the way those young men overcome many obstacles to live happy, fulfilling lives.

Upcoming interviews will feature: Professor Rachelle Crosbie-Watson from the University of California, Los Angeles, who teaches the first university course focused entirely on Duchenne; Dr. Ron Victor, a Cedars-Sinai cardiologist and researcher looking at the benefits of Cialis and Viagra for Duchenne cardiomyopathy; and, Scotty Bob Morgan, a daredevil wingsuit pilot, who has raised awareness worldwide about Duchenne, flying a specially made Coalition Duchenne wingsuit.

About Duchenne muscular dystrophy: Duchenne muscular dystrophy is a progressive muscle wasting disease. It is the most common fatal disease that affects children. Duchenne occurs in 1 in 3,500 male births, across all races, cultures and countries. Duchenne is caused by a defect in the gene that codes for the protein dystrophin. This is a vital protein that helps connect the muscle fiber to the cell membranes. Without dystrophin, the muscle cells become unstable, are weakened and lose their functionality. Life expectancy ranges from the mid teenage years to the mid 20s. Their minds are unaffected.

About Coalition Duchenne: Jayasuriya founded Coalition Duchenne in 2010 (http://www.coalitionduchenne.org) to raise global awareness for Duchenne muscular dystrophy, to fund research and to find a cure for Duchenne. Coalition Duchenne is a 501c3 non-profit corporation.

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Coalition Duchenne Launches Youtube Interview Series 'Making a Difference in Duchenne'

The growing number of biological structures being grown on chips in various laboratories around the world is rapidly replicating the entire gamut of major human organs. Now one of the most important of all a viable functioning heart has been added to that list by researchers at the University of California at Berkeley (UC Berkeley) who have taken adult stem cells and grown a lattice of pulsing human heart tissue on a silicon device.

Sourced from human-induced pluripotent stem cells able to be persuaded into forming many different types of tissue, the human heart device cells are not simply separate groups of cells existing in a petri dish, but a connected series of living cells molded into a structure that is able to beat and react just like the real thing.

"This system is not a simple cell culture where tissue is being bathed in a static bath of liquid," said study lead author Anurag Mathur, a postdoctoral researcher at UC Berkeley. "We designed this system so that it is dynamic; it replicates how tissue in our bodies actually gets exposed to nutrients and drugs."

Touted as a possible replacement for living animal hearts in drug-safety screening, the ability to easily access and rapidly analyze a heart equivalent in experiments presents appealing advantages.

"Ultimately, these chips could replace the use of animals to screen drugs for safety and efficacy," said professor of bioengineering at UC Berkeley, and leader of the research team, Kevin Healy.

The cardiac microphysiological system, as the team calls its heart-on-a-chip, has been designed so that its silicon support structure is equivalent to the arrangement and positioning of conjoining tissue filaments in a human heart. To this supporting arrangement, the researchers loaded the engineered human heart cells into the priming tube, whose cone-shaped funnel assisted in aligning the cells in a number of layers and in one direction.

In this setup, the team created microfluidic channels on each side of the cell holding region to replicate blood vessels to imitate the interchange of nutrients and drugs by diffusion in human tissue. The researchers believe that this arrangement may also one day provide the ability to view and gauge the expulsion of metabolic waste from the cells in future experiments.

"Many cardiovascular drugs target those channels, so these differences often result in inefficient and costly experiments that do not provide accurate answers about the toxicity of a drug in humans," said Professor Healy. "It takes about US$5 billion on average to develop a drug, and 60 percent of that figure comes from upfront costs in the research and development phase. Using a well-designed model of a human organ could significantly cut the cost and time of bringing a new drug to market."

The use of animal organs to forecast human reactions to new drugs is problematic, the UC Berkeley researchers note, citing the fundamental differences between species as being responsible for high failure rates in using these models. One aspect responsible for this failure is to be found in the difference in the ion channel structure between human and other animals where heart cells conduct electrical currents at different rates and intensities. It is the standardized nature of using actual human heart cells that the team sees as the heart-on-a-chip's distinct advantage over animal models.

The UC Berkeley device is certainly not the first replication of an organ-on-a-chip, but potentially one of the first successful ones to integrate living cells and artificial structures in a single functioning unit. Harvard's spleen-on-a-chip, for example, replicates the operation of the spleen, but does so by using a set of circulatory tubes containing magnetic nanobeads.

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Heart-on-a-chip beats a steady rhythm

Lindsey Caldwell

Heart disease is the leading cause of death among Americans. Recently the bio-tech industry has been exploding with cardiac research like last week's heart attack preventing nanobots. New research by the team at the University of California, Berkley has created working human heart cells on a tiny chip designed to test the efficacy of new drugs in clinical trials. This heart-on-a-chip is officially known as a cardiac microphysiological system, or MPS. Using this heart-on-a-chip, scientists can measure the potential cardiac damage of a drug before it reaches expensive human trials.

Drug trials can take years, and to mitigate risk these drugs undergo testing in non-human subjects. Animals are often used in place of humans, but animal models can be problematic. Specifically, they are less effective at predicting cardiotoxicity, wherein a drug damages the heart. This is important because one-third of drugs withdrawn from testing are pulled due to cardiotoxic effects.

Drugs that are first tested in animal models can succeed to future testing stages without setting off alarms. After successful early stages more time and money is invested and the drugs progress to human trials, only to be stopped in their tracks because they are found to be toxic to human hearts.

The cells on this tiny MPS chip are human heart cells that were created from pluripotent stem cells. These cells react to drugs the same way as a human heart inside a living person. By creating a portable, low-risk, and accurate drug testing environment, scientists may be able to advance clinical trials of new drugs and bring them to market sooner.

Here is a video by the UC Berkley research team of their heart cells actually beating.

Source: Berkeley

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Heart-on-a-chip tests drugs cardiotoxicity with its real heartbeat