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Objectives To characterize the activation of platelet integrin αⅡbβ3 induced by two anti-human platelet tetraspanin monoclonal antibodies (mAbs), HI117 and SJ9A4, and investigate their potential mechanism of action. Methods Using 125 I-labeled human fibrinogen (Fg), specific Fg binding to human platelets induced by HI117 and SJ9A4 was measured. Results HI117 and SJ9A4 (10μg/ml and 20μg/ml) induced specific Fg binding to human platelets, suggesting that the two mAbs evoked activation of platelet integrin αⅡbβ3. Further study indicated that HI117 and SJ9A4 induced integrin αⅡbβ3 activation independent of platelet Fc-receptors, and that HI117 and SJ9A4-induced integrin αⅡbβ3 activation was inhibited by pretreatment of platelets with sphingosine, aspirin, apyrase, and/or PGI2. Conclusions Anti-platelet tetraspanin (CD9) mAbs, HI117 and SJ9A4, can induce platelet integrin αⅡbβ3 activation independent of Fc-receptors. Three signaling pathways, namely thromboxane, secreted ADP, and cAMP pathways, may be involved in the process, with protein kinase C activation presumably being the common step of the three pathways. 相似文献
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INTRODUCTION CD9antigen(Ag)isa 2 4 kDmembraneglycoproteinexpressedonthesurfaceofhumanplateletsaswellasonthesurfaceoflymphoidprogenitorcells ,pre Bcellleukemiaandothercelltypes.Thisproteinbelongstoarecentlydelin eatedfamilyofcell surfaceAgsthatspanthemembra… 相似文献
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纤维蛋白原基因调控的研究进展 总被引:3,自引:0,他引:3
纤维蛋白原基因调控的研究进展侯庆明综述李家增审校纤维蛋白原是一种重要的血浆糖蛋白,属于Ⅱ类肝性急性相蛋白(classⅡhepaticacutephaseproteins)。它主要通过以下途径参与血液调节:①受凝血酶作用形成纤维蛋白多聚体;②与血小板膜... 相似文献
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先天性出血性疾病中最常见的是血友病甲。人们很早就发现了血友病,而且随着凝血试验方法的建立和改进,将血友病分为甲,乙,丙三型,并明确了其所缺失的凝血因子。但是,随着免疫学,生物化学及分子生物学的发展,发现与各型血友病有关的凝血因子在不同个体中有不同的特点。早期免疫学检测有交叉反应阳性(CRM~ )和阴性(CRM~-)之分,这意味着在一些个体中与其疾病相关的因子并不缺失 相似文献
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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。 相似文献
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ANTI-HUMAN PLATELET TETRASPANIN (CD9) MONOCLONAL ANTIBODIES INDUCE PLATELET INTEGRIN αⅡbβ3 ACTIVATION IN A Fc RECEPTOR-INDEPENDENT FASHION 总被引:2,自引:0,他引:2
Objective. This study characterized the activation of platelet integrin αⅡbβ3 induced by two anti-human platelet te-traspanin monoclonal antibodies(mAbs),HI117 and SJ9A4.Methods. Using ^125I-labeled human fibrinogen (Fg) ,specific Fg binding to human platelets induced by HI117 and SJ9A4 was measured as indication of activation of platelet integrin αⅡbβ3 by the two mAbs. Results. HI117 and SJ9A4( 10μg/ml and 20μg/ml) induced evident specific Fg binding to human platelets,sug-gesting that the two mAbs evoked activation of platelet integrin αⅡbβ3. Further study indicated that HI117 and SJ9A4 induced integrin αⅡbβ3 activation independent of platelet Fc-receptors, and that HI117 and SJ9A4-induced integrin αⅡbβ3 activation was inhibited by sphingosing, aspirin, apyrase, and/or PGI2. Condusion. The anti-platelet tetraspanin(CD9) mAbs, HI117 and SJ9A4, can induce platelet integrin αⅡbβ3 acti-vation independent of Fc-receptors, Three signaling pathways, i, e. thromboxane, secreted ADP, and cAMP pathways may be involved in the process, with protein kinase C activation presumably being the common step of the three pathways. 相似文献