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Platelet death in thrombosis and thrombocytopenia

– Group Leader

Fellow in Pharmacology Jesus College


E-Mail:  Tel: +44 1223 334032/334024
Fax: +44 1223 334100

Keywords

Thrombosis, Thrombocytopenia, Platelets, Cancer chemotherapy, Cellular signalling, Cell death, Calcium ,Apoptosis, Necrosis. Phosphatidylserine exposure

Investigator Biography

Matthew read natural sciences at Cambridge and stayed to complete a PhD with Stewart Sage (Department of Physiology, Development and Neuroscience) on the regulation of calcium signalling in platelets. He moved to Alastair Poole’s group in Bristol to work on platelet granule secretion and thrombosis. He is on the Editorial Board of the Journal of Thrombosis and Haemostasis, and the Editorial Advisory Panel of the Biochemical Journal. In 2015 he was appointed to a lectureship in the Pharmacology Department. His current research focuses on the triggers of platelet death, how it is controlled, and the role that it plays in thrombosis and thrombocytopenia.

 

Key publications

Harper MT, Camacho Londono JE, Quick K, Camacho Londono J, Philipp SE, Birnbaumer L, Freichel M, Poole AW (2013). Transient receptor potential channels function as a coincidence signal detector mediated phosphatidylserine exposure. Science Signalling, 6, ra50.

Harper MT, Poole AW. Chloride channels are necessary for full platelet phosphatidylserine exposure and procoagulant activity. Cell Death Dis, 4, e969.

Harper MT, Poole AW (2012). Bcl-xL –inhibitory BH3 mimetic ABT-737 depletes platelet calcium stores. Blood, 119, 4337-4338.

Harper MT, Poole AW (2011). Contribution of store-operated calcium entry and non-capacitative calcium entry to thrombin-induced calcium signalling in human platelets. Cell Calcium, 50, 351-358.

Harper MT, Poole AW (2011). PKC inhibition enhances Ca2+ signalling and phosphatidylserine exposure downstream of protease-activated receptor-1 but not protease-activated receptor-4 in human platelets. J Thromb Haemost, 9, 1599-1607.

 

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