How is the activation of platelets controlled in health and disease?

The role of adenylyl cyclase 6 in platelet function, haemostasis and thrombosis (Miss Bethany Webb)

Researching how blood clotting escapes the normal controls in people with heart disease. Platelets are blood cells that become ‘sticky’ and clump together to form blood clots that stop us from bleeding too much after injury. However, in people with coronary heart disease, platelets also form blood clots inside the coronary arteries, leading to heart attacks. Normally, blood vessels release a chemical called prostacyclin, which initiates other signals to stop platelets from becoming sticky until they are needed in response to an injury. However, this system is ineffective in diseased arteries, and these researchers want to find out why. Studying blood samples has revealed that platelets from people at risk of heart disease do not respond very well to prostacyclin. To work properly, prostacyclin must activate proteins called adenylyl cyclases (ACs) on the surface of the platelets. Professor Khalid Naseem and his team of researchers have discovered that one type of AC – AC6 – may be the key protein that stops platelets becoming too sticky in response to prostacyclin. In this study they will use mice to separate platelets from the blood and use a number of laboratory methods to understand how AC6 stops the cells getting sticky. A better understanding of this process will help doctors understand how and why heart disease disrupts the usual control of platelets, and to develop new medicines to prevent heart attack.