F. Stierlin, F. Molica, J. Reny, B. Kwak, P. Fontana
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引用次数: 11
摘要
Pannexin1 (Panx1)是一种膜通道形成蛋白,允许小分子(如ATP)通过,在人血小板中表达。最近,我们发现抑制Panx1会影响胶原诱导的血小板聚集,但不会影响其他激动剂引发的血小板聚集。我们还发现单核苷酸多态性(SNP;rs1138800)在Panx1基因中编码一个功能获得通道(Panx1- 400c),并与胶原诱导的血小板反应性增强有关。在这项研究中,我们评估了来自ADRIE研究的758名接受阿司匹林和/或氯吡格雷治疗的稳定心血管患者的SNP与血小板反应性的关系。我们发现,在稳定性心血管患者中,Panx1-400C等位基因的存在与血小板反应性无关,与使用血小板聚集激动剂(胶原蛋白、ADP或花生四烯酸)或抗血小板药物方案无关。此外,Panx1-400A > C SNP也不影响相同稳定心血管患者队列中心脏缺血事件的再发生。
Pannexin1 Single Nucleotide Polymorphism and Platelet Reactivity in a Cohort of Cardiovascular Patients
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.
期刊介绍:
Cessation
Cell Communication and Adhesion is an international Open Access journal which provides a central forum for research on mechanisms underlying cellular signalling and adhesion. The journal provides a single source of information concerning all forms of cellular communication, cell junctions, adhesion molecules and families of receptors from diverse biological systems.
The journal welcomes submission of original research articles, reviews, short communications and conference reports.