FREE RADICAL-MEDIATED PLATELET ACTIVATION BY HEMOGLOBIN RELEASED FROM RED-BLOOD-CELLS
FREE RADICAL-MEDIATED PLATELET ACTIVATION BY HEMOGLOBIN RELEASED FROM RED-BLOOD-CELLS
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DOI：
10.1016/0003-9861(92)90267-z
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发表时间：
1992-12-01
影响因子：
3.9
通讯作者：
BALSANO, F
中科院分区：
文献类型：
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作者：
IULIANO, L;VIOLI, F;BALSANO, F
众所周知，血栓形成的速度取决于血小板和红细胞之间的相互作用，但这一过程的机制仍不清楚。我们在这里表明，从受损的红细胞中释放的纳摩尔水平的血红蛋白可以诱导血小板聚集。分子机制不是基于受体的，而是涉及血小板衍生的过氧化氢氧化氧合血红蛋白，随后产生一种小的未知自由基物质，通过ESR光谱检测。高铁血红蛋白和一氧化碳处理的血红蛋白不能引起血小板活化或自由基形成。血红蛋白诱导的血小板聚集可被过氧化氢酶或自由基清除剂完全阻断。这些发现表明了一种新的细胞外自由基第二信使在血小板活化中的作用。
It is known that the rate of thrombus formation depends on interaction between platelets and erythrocytes, but the mechanism of this process has remained obscure. We here show that nanomolar levels of hemoglobin released from damaged red blood cells can induce platelet aggregation. The molecular mechanism is not receptor-based, but involves oxidation of oxyhemoglobin by platelet-derived hydrogen peroxide, with subsequent generation of a small unknown free radical species, detected by ESR spectroscopy. Methemoglobin and carbon monoxide-treated hemoglobin are unable to cause platelet activation or radical formation. The aggregation of platelets induced by hemoglobin is completely blocked by catalase or radical scavengers. These findings indicate a role for a novel extracellular free radical second messenger in the activation of platelets.