IMPC: Analysis of the role of Cx57 in the regulation of platelet function, haemostasis and thrombosis

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Platelets are small cells that control blood clotting. When they encounter cuts or damage to blood vessels they rapidly become sticky and stick to each other. This forms a plug, the first stage of clot formation that stops the bleeding as quickly as possible. Blood vessels become abnormal in cardiovascular disease and platelets can mistake these diseased vessels for cut vessels and consequently trigger the blood to form clots inside blood vessels (this is also known as thrombosis). This can clog up arteries and is the main trigger for heart attacks and strokes, which are frequently fatal. Scientists' successes in identifying how platelets sense healthy and damaged blood vessels, and also communicate with each other, has been critical in developing more effective drugs to prevent heart attacks and strokes, although such cardiovascular diseases still represent the principal causes of death in the UK. We are therefore focussing on increasing our understanding of the molecules and processes that enable platelets to be controlled in order to develop more effective medicines. We
have recently found a new protein called Cx57 on platelets and have produced considerable data to show that this is likely to contribute to thrombosis. In order to confirm this we need to study platelets that do not have this protein. In this project we will use mice that have been genetically engineered to lack Cx57. We will test what effect this has on platelet function, bleeding and thrombosis. This will form an important step to determine whether drugs that target this protein may be successful in preventing thrombosis and the other diseases in which platelets are involved.