硫酸乙酰肝素从内皮细胞的释放。对超急性排斥反应发病机制的影响。
Release of heparan sulfate from endothelial cells. Implications for pathogenesis of hyperacute rejection.
作者信息
Platt J L, Vercellotti G M, Lindman B J, Oegema T R, Bach F H, Dalmasso A P
机构信息
Department of Pediatrics, University of Minnesota, Minneapolis 55455.
出版信息
J Exp Med. 1990 Apr 1;171(4):1363-8. doi: 10.1084/jem.171.4.1363.
Abstract
Heparan sulfate proteoglycan associated with endothelial cells in normal blood vessels inhibits intravascular coagulation and egress of blood cells and plasma proteins, key features of hyperacute rejection. It was shown herein that exposure of cultured porcine endothelium to human serum as a source of natural antibodies and complement caused cleavage and release of 5% of endothelial cell proteoglycans within 4 min and greater than 50% within 1 h. Proteoglycan release depended on activation of the classical complement pathway and preceded irreversible cell injury. These findings suggest that loss of endothelial cell proteoglycan may be a critical step in the pathogenesis of hyperacute rejection and in diseases involving humoral injury to endothelial cells.
摘要
正常血管中与内皮细胞相关的硫酸乙酰肝素蛋白聚糖可抑制血管内凝血以及血细胞和血浆蛋白的渗出，而这正是超急性排斥反应的关键特征。本文研究表明，将培养的猪内皮细胞暴露于作为天然抗体和补体来源的人血清中，4分钟内5%的内皮细胞蛋白聚糖会发生裂解和释放，1小时内释放量超过50%。蛋白聚糖的释放依赖于经典补体途径的激活，且先于不可逆的细胞损伤。这些发现表明，内皮细胞蛋白聚糖的丧失可能是超急性排斥反应发病机制以及涉及内皮细胞体液损伤的疾病中的关键步骤。
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