Abstract
Pannexin1 (Panx1), a membrane channel-forming protein permitting the passage of small-sized molecules, such as ATP, is expressed in human platelets. Recently, we showed that inhibiting Panx1 affects collagen-induced platelet aggregation but not aggregation triggered by other agonists. We also found that a single nucleotide polymorphism (SNP; rs1138800) in the Panx1 gene encoded for a gain-of-function channel (Panx1-400C) and was associated with enhanced collageninduced platelet reactivity. Here, we assessed the association of this SNP with platelet reactivity in a cohort of 758 stable cardiovascular patients from the ADRIE study treated with aspirin and/ or clopidogrel. We found that presence of the Panx1-400C allele was not associated with platelet reactivity in stable cardiovascular patients, irrespective of the platelet aggregation agonist used (collagen, ADP or arachidonic acid) or the anti-platelet drug regimen. Moreover, the Panx1-400A>C SNP did also not affect the re-occurrence of cardiac ischemic events in the same stable cardiovascular patient cohort.
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Stierlin, F. B., Molica, F., Reny, J. L., Kwak, B. R., & Fontana, P. (2017). Pannexin1 single nucleotide polymorphism and platelet reactivity in a Cohort of cardiovascular patients. Cell Communication and Adhesion, 23(1), 11–15. https://doi.org/10.1080/15419061.2017.1282469
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