PKC alpha: a critical protein for forming blood clots

Protein kinase C-dependent platelet secretion: central regulator of thrombosis and atherogenesis: renewal

Platelets are small cells in the bloodstream that clump together at sites of injury, triggering a clot to form to prevent excessive bleeding. Platelet clumping can be activated in diseased arteries when a fatty plaque ruptures. When this happens in a coronary artery which supplies the heart muscle, it causes a heart attack. When platelets adhere to sites of injury in the bloodstream they activate ‘sticky’ proteins on their surface that make them clump together. They secrete chemical signals that activate nearby platelets, so that a plug forms very rapidly to stop the flow of blood. Receptor molecules on the platelet’s surface sense chemicals in its environment and control the cell’s activity through a central regulator: a protein called PKC alpha. Professor Alastair Poole’s BHF-funded research has revealed the crucial role of PKC alpha in the regulation of platelets. His team will now hunt for genes and proteins that get switched on by PKC alpha. They will investigate the role of target genes by eliminating them in mice. They will also study human patients who have mutations in these genes. Prof Poole has found that by controlling which chemicals platelets secrete, PKC alpha also regulates how plaques develop in arteries. He will study this role further in mice. By better understanding how platelets are regulated, we will have a better picture of which receptors could be targets for drugs that stop blood clots. This may lead to new treatments to prevent heart attacks.