Belisario M A, Tafuri S, Di Domenico C, Squillacioti C, Della Morte R, Lucisano A, Staiano N
Dipartimento di Biochimica e Biotecnologie Mediche, Università di Napoli Federico II, Via S. Pansini 5, 80131, Naples, Italy.
Biochim Biophys Acta. 2000 Feb 2;1495(2):183-93. doi: 10.1016/s0167-4889(99)00160-3.
Platelets represent a target of reactive oxygen species produced under oxidative stress conditions. Controversial data on the effect of these species on platelet functions have been reported so far. In this study we evaluated the effect of a wide range of H(2)O(2) concentrations on platelet adhesion to immobilized fibrinogen and on pp72(syk) and pp125(FAK) tyrosine phosphorylation. Our results demonstrate that: (1) H(2)O(2) does not affect the adhesion of unstimulated or apyrase-treated platelets to immobilized fibrinogen; (2) H(2)O(2) does not affect pp72(syk) phosphorylation induced by platelet adhesion to fibrinogen-coated dishes; (3) H(2)O(2) reduces, in a dose-dependent fashion, pp125(FAK) phosphorylation of fibrinogen-adherent platelets; (4) concentrations of H(2)O(2) near to physiological values (10-12 microM) are able to strengthen the subthreshold activation of pp125(FAK) induced by epinephrine in apyrase-treated platelets; (5) H(2)O(2) doses higher than 0.1 mM inhibit ADP-induced platelet aggregation and dense granule secretion. The ability of H(2)O(2) to modulate pp125(FAK) phosphorylation suggests a role of this molecule in physiological hemostasis as well as in thrombus generation.
血小板是氧化应激条件下产生的活性氧的作用靶点。迄今为止，关于这些活性氧对血小板功能影响的数据存在争议。在本研究中，我们评估了广泛浓度范围的过氧化氢（H₂O₂）对血小板与固定化纤维蛋白原黏附以及对pp72(syk)和pp125(FAK)酪氨酸磷酸化的影响。我们的结果表明：（1）H₂O₂不影响未刺激的或经腺苷三磷酸双磷酸酶（apyrase）处理的血小板与固定化纤维蛋白原的黏附；（2）H₂O₂不影响血小板黏附于纤维蛋白原包被培养皿所诱导的pp72(syk)磷酸化；（3）H₂O₂以剂量依赖方式降低纤维蛋白原黏附血小板的pp125(FAK)磷酸化；（4）接近生理值（10 - 12微摩尔）的H₂O₂浓度能够增强肾上腺素在经apyrase处理的血小板中诱导的pp125(FAK)亚阈值激活；（5）高于0.1毫摩尔的H₂O₂剂量抑制二磷酸腺苷（ADP）诱导的血小板聚集和致密颗粒分泌。H₂O₂调节pp125(FAK)磷酸化的能力表明该分子在生理止血以及血栓形成中起作用。
