gp91phox-dependent expression of platelet CD40 ligand
gp91phox-dependent expression of platelet CD40 ligand
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DOI：
10.1161/01.cir.0000134963.77201.55
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发表时间：
2004-09-01
期刊：
影响因子：
37.8
通讯作者：
Violi, F
中科院分区：
文献类型：
--
作者：
Pignatelli, P;Sanguigni, V;Violi, F
背景-CD 40配体（CD 40 L）的表达对血小板是介导的激动剂，但潜在的机制仍不清楚。方法和结果-CD 40 L的表达进行了测量，从健康受试者的血小板，有和没有添加抗氧化剂或磷脂酶A2（PLA 2）抑制剂和血小板从2例gp 91 phox的遗传缺陷。免疫沉淀分析也进行，以确定是否正常血小板显示gp 91 phox表达。与过氧化氢酶和甘露醇不同，超氧化物歧化酶抑制健康受试者中激动剂诱导的血小板CD 40 L表达。免疫沉淀分析也表明，健康受试者的血小板表达gp 91 phox。在2名男性患者遗传性gp 91 phox缺陷，胶原，凝血酶，花生四烯酸刺激的血小板显示几乎完全没有超氧阴离子（O-2（-））和CD 40 L的表达。从健康受试者的血小板与PLA 2抑制剂几乎完全防止激动剂诱导的O-2（-）和CD 40 L expressions.Conclusions-These数据提供的第一个证据表明，血小板CD 40 L的表达发生通过花生四烯酸介导的gp 91 phox激活。
Background-CD40 ligand (CD40L) expression on platelets is mediated by agonists, but the underlying mechanism is still unclear.Methods and Results-CD40L expression was measured in platelets from healthy subjects both with and without the addition of antioxidants or a phospholipase A2 (PLA2) inhibitor and in platelets from 2 patients with an inherited deficiency of gp91phox. Immunoprecipitation analysis was also performed to determine whether normal platelets showed gp91phox expression. Unlike catalase and mannitol, superoxide dismutase inhibited agonist-induced platelet CD40L expression in healthy subjects. Immunoprecipitation analysis also showed that platelets from healthy subjects expressed gp91phox. In 2 male patients with inherited gp91phox deficiency, collagen-, thrombin-, and arachidonic acid-stimulated platelets showed an almost complete absence of superoxide anion (O-2(-)) and CD40L expression. Incubation of platelets from healthy subjects with a PLA2 inhibitor almost completely prevented agonist-induced O-2(-) and CD40L expression.Conclusions-These data provide the first evidence that platelet CD40L expression occurs via arachidonic acid-mediated gp91phox activation.