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Pannexin1 Single Nucleotide Polymorphism and Platelet Reactivity in a Cohort of Cardiovascular Patients
Authors:Florian B. Stierlin  Filippo Molica  Jean-Luc Reny  Pierre Fontana
Affiliation:1. Department of Pathology and Immunology, University of Geneva, Geneva, Switzerland;2. Department of Medical Specializations – Cardiology, University of Geneva, Geneva, Switzerland;3. Geneva Platelet Group, University of Geneva, Geneva, Switzerland;4. Geneva Platelet Group, University of Geneva, Geneva, Switzerland;5. Department of Medical Specializations, Division of Internal Medicine and Rehabilitation, Trois-Chêne Hospital, Geneva University Hospitals, Geneva, Switzerland;6. Department of Medical Specializations, Division of Angiology and Haemostasis, Geneva University Hospitals, Geneva, Switzerland
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 collagen-induced 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.
Keywords:Platelet aggregation  genetic polymorphism  pannexin1  membrane channel  anti-platelet drugs  collagen
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