OTTAWA Growing up in Stellarton, Dr. Lynn Megeney didnt really know what a scientist was or did.

Dr. Lynn Megeney, originally of Stellarton, discovered that proteins involved in cell death also play a key role in abnormal heart muscle thickening. The scientist, who obtained his undergrad at St. FX, conducted his research at Ottawa Hospital Research Institute and the University of Ottawa. SUBMITTED

Years later however, Megeney, now a scientist, is making advances in important aspects of cardiology.

While most people would consider a big heart to be a good thing, for heart disease experts, it is often a sign of serious disease. Megeney made the surprising discovery at the Ottawa Hospital Research Institute and the University of Ottawa. He discovered that proteins involved in cell death also play a key role in abnormal heart muscle thickening.

The research, published in the Oct. 7, 2013, online edition of Proceedings of the National Academy of Sciences (PNAS), could lead to new treatments for certain forms of heart disease.

Heart muscle thickening, called cardiac hypertrophy, can be a healthy response to exercise and pregnancy, said Megeney. However, it often occurs in people with high blood pressure, diabetes, heart failure and certain genetic conditions.

In these people, roughly 15 per cent of the population, the heart can easily grow twice as large as normal due to an increase in the size of individual heart muscle cells. Too much growth can lead to increased stiffness and reduced blood supply, and eventually reduced pumping function and heart failure.

Several years ago, Megeney noticed that heart muscle cells undergoing this kind of abnormal growth had many similarities with cells that are beginning to undergo an orderly form of cell suicide called programmed cell death. In the current research paper, Megeney and his team show that blocking the proteins that control this form of cell death also blocks abnormal heart muscle thickening.

Megeney and his team exposed rats to a number of different drugs that each induce abnormal heart muscle thickening. The rats were then given a form of experimental gene therapy to block cell suicide proteins in the heart. Three weeks later, the rats that received the experimental therapy had much smaller heart muscle cells (37 per cent smaller than those that did not receive the therapy), and smaller hearts overall. In fact, the disease model rats that received the experimental therapy seemed just as healthy as normal rats.

Our research shows, for the first time, that heart muscle cells use the same molecular machinery for unhealthy growth as they would use to commit suicide, said Megeney. This may seem quite surprising to some people, but it fits with a growing body of research showing that cell death proteins can play many other roles in the body.

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Dr. Lynn Megeney’s research on heart thickness cutting edge

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