Disparity in blood clotting mechanisms can contribute to the pathogenesis of stroke and ischemic heart diseases in the African-American population, according to the latest research conducted by scientists at Baylor College of Medicine, in collaboration with research team of Jefferson Medical College of Thomas Jefferson University in Philadelphia.
Statistics indicate that the overall risk of ischemic heart disease and stroke is highest in the African-American population when compared to any other race in United States. Although, various factors contribute to this high prevalence and racial disparity, such as availability of healthcare resources, economic status, and other environmental factors. However, the latest research indicated that the difference in platelet response is also an important factor.
According to the results of research published in Nature Medicine, BCM researcher Dr. Chad Shaw and Jefferson Medical College researcher Paul Bray, along with several other colleagues, explained the racial differences in the reactivity of platelets along with specialized proteins that affect the speed of platelet activation. These proteins include phosphatidylcholine transfer protein (abbreviated as PC-TP) along with other receptors required for thrombin activation.
Details of the research:
The research team compared the blood samples of 84 caucasians and 70 African-American subjects to identify that the speed of clotting was very high in the later group (with even faster speed in the presence of thrombin). Thrombin is known to activate the activation of platelets by stimulating PAR4.
Dr. Shaw, the corresponding author of the published report and assistant professor of molecular and human genetics at BCM, suggested that this difference can be explained on the basis of racial factors. The research time identified that the expression of PC-TP can be controlled by a microRNA (miR-376c) in order to minimize the activity of PAR4 (thrombin activation receptors). This special mRNA is more concentrated in the blood of white study subjects as compared to African-Americans.
Shaw suggested that the research will help in devising specialized therapeutic regimens to prevent abnormal clot formation (like aspirin, which exerts its protective functions by interfering with the activity of platelets in the clot formation). Many other pharmacological interventions are underway that deals with the monitoring the activity of platelet PAR1 — a chemical fairly similar in structure and function to PAR4. The research team of BCM-Jefferson also discovered that inhibition of PAR1 can allow thrombin to further activate PAR4 in African American individuals.
Shaw explained how important it is to understand different mechanisms that can affect the response to the treatment. He also suggested that the choice of personalized treatment helps in achieving quality results.
The study was funded by Cardeza Foundation for Hematologic Research and the National Institutes of Health.