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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


Thrombosis, Thrombocytopenia, Platelets, Cancer chemotherapy, Cellular signalling, Cell death, Calcium, Apoptosis, Necrosis, Phosphatidylserine exposure, 3Rs


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. Matthew is on the editorial board of the journals Platelets, Scientific Reports and Pharmacology Reviews and Perspectives, and is a founding trustee of The Platelet Society, a charity that promotes research and education about the roles of platelets in disease. In 2015 he was appointed to a lectureship in the Pharmacology Department. His current research focuses on understanding platelets in health and disease.
Matthew is a Fellow of Jesus College, Cambridge, where he supervises second year medics and vets taking the MoDA course. He is also the Admissions Tutor for Sciences. Queries related to undergraduate admissions should be directed at Cambridge Admissions Office or the


Lab members

Harper Lab summer 2018


Key publications

Wei H, Harper MT (2019). ABT-737 triggers caspase-dependent inhibition of platelet procoagulant extracellular vesicle release during apoptosis and secondary necrosis in vitro. Thromb Haemost, In Press

Wei H, Malcor JM, Harper MT (2018). Lipid rafts are essential for release of phosphatidylserine-exposing extracellular vesicles from platelets. Sci Rep, 8, 9987. 

Harper MT (2017). Auranofin, a thioredoxin reductase inhibitor, causes platelet death through calcium overload. Platelets, In Press

Harper MT, van den Bosch MT, Hers I, Poole AW (2015). Platelet dense granule secretion defects may obscure our understanding of α-granule secretion mechanisms. Blood, 125, 3034-3036.

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.




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Former lab members

Dr Bonita Apta - Grace Atkinson - Lottie Arnold - Jasmine Bawa - James Brice - Shirom Chabra - Dr Jessica Davies - Lana Huang - Rebecca Gilchirst - Evonne Gaw - Celine Goh - Zhiyuan Lin - Wenxin Ma - Alice Sowton