More than two decades of research on how platelets in the blood become activated and stick together to form clots has given Satya P. Kunapuli, PhD, Professor of Physiology, Professor of Pharmacology and Director of the Sol Sherry Thrombosis Research Center at the Lewis Katz School of Medicine at Temple University, extensive insight into the role of abnormal clot formation in cardiovascular disease.

But the answer to one question has remained elusive: how do platelets – normally spurred into action by cell signaling pathways associated with bleeding – become activated to form clots that ultimately lead to cardiovascular diseases like stroke and heart attack? Now, thanks to a new 7-year, multi-million dollar grant from the National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health, Dr. Kunapuli will be able to focus his research on this fundamental question. The possible answers he discovers could open the way to the development of new preventative strategies and drug therapies for cardiovascular disease.

“Advancing our knowledge of the signaling mechanisms involved in abnormal platelet activation is essential for understanding, treating, and preventing potentially catastrophic cardiovascular events such as stroke,” Dr. Kunapuli said.

The new grant, an NHLBI R35 award, recognizes outstanding investigators who have demonstrated their ability to make significant contributions to cardiovascular research. Dr. Kunapuli’s laboratory has done just that, having made multiple discoveries pertaining specifically to molecular mechanisms underlying platelet activation. Among his team’s breakthroughs was the identification of adenosine diphosphate (ADP) receptor molecules that play an essential role in platelet shape change and aggregation.

Moreover, the R35 award is unique because of the long-term support and flexibility that it provides. Funded with $950,000 each year, over a period of seven years, Dr. Kunapuli will have the freedom to take previous findings in new directions and to conduct research over an extended timeframe. Shorter-duration grants generally do not allow for such open-ended work.

“With the funding, we plan to apply proteomics and genomics approaches to the study of platelets isolated from healthy human subjects,” Dr. Kunapuli explained. In the absence of medications and disease, his team can make clear comparisons of platelets from many healthy individuals and more readily identify true differences in platelet genes and proteins. The discovery of molecular differences could facilitate the discovery of previously unknown signaling pathways and modes of platelet activation that are relevant to cardiovascular disease.

Research reported in this publication was supported by the National Heart, Lung, and Blood Institute of the National Institutes of Health under Award Number R35HL155694. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.