Dr. Peter Liu and Dr. Katey Rayner Awarded Heart & Stroke Foundation Grants

Heart Institute researchers were awarded national peer reviewed Heart and Stroke Foundation Grants-in-Aid!  Dr. Katey Rayner and Dr. Peter Liu received these operating grants in support of their important, novel research that will lead to improved heart health for Canadians. Congratulations to Dr. Rayner and Dr. Liu!

Dr. Peter Liu, Chief Scientific Officer, VP Research, and Clinician Scientist, University of Ottawa Heart Institute

Project: Exosomal Troponin in Heart Failure – A Biomarker and A Biomodulator?
Led by: Peter Liu, MD

Heart attack and heart failure are the most common, and the most devastating cardiovascular conditions. Over 75,000 Canadians each year are newly diagnosed with a heart attack. The diagnosis for heart attack is critically dependent on a special blood test looking for leakage of a protein from heart cells into the bloodstream-the “troponin” test.

Heart failure on the other hand is caused by changes in the shape and function of the heart, due to previous damage, leading to weakened function. Over 600,000 Canadians are afflicted with heart failure, the most rapidly rising chronic heart condition and one in five people with the condition will die within one year of diagnosis.

With advances in technology and the improved “troponin” test recently available worldwide to diagnose heart attack better, we are now faced with a new challenge. The new, super sensitive “troponin” test can diagnose a small heart attack within three hours of onset. With this new tool, greater than 90% of heart failure patients now also have a positive “troponin” test, and this could easily be misdiagnosed as a heart attack. There is now a potential confusion in diagnosis.

Dr. Liu and his team were awarded a Heart and Stroke Foundation Grant-in-Aid to address this new challenge. The team has already uncovered that the troponin released in heart failure is often contained in little membrane packages, called “exosomes” (conversely, the troponin released in a heart attack is free floating in the bloodstream). They have also determined that in heart failure, when the heart is changing shape, troponin is released in abundance in these “exosome” packages. In this project, the team will aim to identify what triggers heart cells to send out these troponin packages, evaluate the various types of heart shape changing forces on heart cells, and importantly, to determine the relative amount of “exosome” troponin vs. free troponin in a heart attack. They will also evaluate the biologic function of the troponin packages to better understand the shape-function coordination network in the heart. The results are expected to generate novel and exciting insights into heart failure, and potentially inform an entirely new way to distinguish a heart attack from heart failure.

Dr. Katey Rayner, Scientist, University of Ottawa Heart Institute

Project: Balance of inflammatory cell death and resolution pathways in atherosclerosis
Led by: 
Katey Rayner, PhD

Atherosclerosis is a disease in which plaque, or atherosclerotic lesion, builds up in the arteries and causes blockage. To regress atherosclerotic lesions, tissue repair and remodeling are needed and these processes require the involvement of anti-inflammatory and pro-reparative pathways.

Dr. Rayner and her team were awarded a Heart and Stroke Grant-in-Aid to find new ways to reduce inflammation within the atherosclerotic plaque and promote lesion regression by targeting cell death pathways. Cell death occurs in different ways in the body, and one method called “necroptosis” causes the cells to explode and release toxic contents into the surrounding area. The Rayner team has previously shown that necroptosis occurs in coronary arteries in patients with severe atherosclerosis. The team has also shown that in a mouse model, necroptosis caused inflammation and lesions in the arteries to grow larger. In this project, the lab will look at how “pro-resolving lipid mediators”, a type of fat that can dampen inflammation and promote tissue repair, reduce necroptotic cell death in a mouse model genetically predisposed to developing atherosclerosis. The team also aims to describe how microRNAs’ are involved in the necroptosis pathway to understand how they control cell viability and inflammation. The goal is to identify ways to turn off necroptosis to reduce inflammation and plaque progression, with a view to develop new therapies that deliver pro-resolution lipids and/or microRNAs to treat atherosclerosis, or new diagnostic tests to better predict and identify individuals who would benefit the most from aggressive anti-inflammatory treatment.

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