Grant: Project Grant

Myocardial infarction (MI), also commonly known as a heart attack, occurs when there is a blockage of a blood vessel supplying oxygen and nutrients to the heart muscles. Current therapy aims at re-establishing the blood flow to protect the heart muscles from further damage. This strategy is effective in the recovery from a heart attack. However, the death of a significant portion of heart cells leads to progressive and substantial loss of heart function resulting in heart failure. Our research focuses on endothelial colony forming cells (ECFCs) that are present in the human blood. These are believed to be the precursor of endothelial cells, which create inner-lining of blood vessels. We recently isolated these cells and injected them into the mice with the heart attack caused by permanent blockage of blood flow to a significant portion of the heart. While the cells reduced damage to heart muscles, the effects were identified to be mediated by nanoparticles released from ECFCs, termed as "exosomes". Exosomes are nanometer-sized vesicles, which are secreted by many cell types in the human body. These vesicles transport genetic material from the cells of their source to the receiver cells. Our current primary research question is: "Can the exosomes repair the heart after myocardial infarction?" To address this question, we first have to decode the genetic message present in the exosomes released from ECFCs. We will carry out a series of animal experiments to understand the exosome cargo, an ideal dose and route of administration, and effects on the heart attack on both sexes. Our research goal is to identify a novel therapeutic intervention for patients with heart attack, which will not only limit the heart damage but will also improve the tissue repair.