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目的 研究 2种抗人血小板tetraspanin单克隆抗体HI117和SJ9A4引起的血小板整合素活化及其机制。方法 用12 5Ⅰ标记的人纤维蛋白原 ,测定HI117和SJ9A4引起的纤维蛋白原与人血小板的特异的结合 ,表明这 2种单抗激活血小板整合素αⅡbβ3。结果 HI117和SJ9A4 ( 10 μg ml和 2 0 μg ml)引起纤维蛋白原与人血小板特异的结合 ,表明这 2种单抗引起血小板整合素αⅡbβ3激活 ,进一步研究表明这种激活不依赖血小板Fc受体 ,而且HI117和SJ9A4引起的血小板整合素αⅡbβ3激活可由于以Sphingosine、Aspirin、αβ、rase和成PGI2 预处理血小板而被抑制。结论 抗人血小板tetraspanin (CD9)单克隆抗体HI117和SJ9A4能引起血小板整合素αⅡbβ3激活且不依赖Fc受体 ,3种信号途径即血栓烷 ,分泌ADP和CAMP途径可能涉及这一过程 ,蛋白激酶C激活可能是这 3个途径的共同步骤。
Objective To investigate the activation of platelet integrin induced by two anti-human tetraspanin monoclonal antibodies HI117 and SJ9A4 and its mechanism. Methods Specific binding of fibrinogen to human platelets induced by HI117 and SJ9A4 was determined using 125I - labeled human fibrinogen, indicating that these two monoclonal antibodies activated platelet integrin αIIbβ3. Results The specific binding of fibrinogen to human platelets was induced by HI117 and SJ9A4 (10 μg ml and 20 μg ml), indicating that these two mAbs cause platelet integrin αⅡbβ3 activation. Further studies indicated that this activation is independent of platelet Fc receptor , And platelet integrin alphaIIbbeta3 activation by HI117 and SJ9A4 can be inhibited by pretreatment of platelets with Sphingosine, Aspirin, alpha beta, rase and PGI2. Conclusion The anti-human platelet tetraspanin monoclonal antibody HI117 and SJ9A4 can induce the platelet integrin αⅡbβ3 activation and not depend on the Fc receptor. The three signaling pathways, thromboxane, and the secretion of ADP and CAMP may be involved in this process. Protein kinase C Activation may be a common step in these 3 ways.