F11-receptor (F11R/JAM) mediates platelet adhesion to endothelial cells: Role in inflammatory thrombosis
F11-receptor (F11R/JAM) mediates platelet adhesion to endothelial cells: Role in inflammatory thrombosis
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DOI：
10.1055/s-0037-1613312
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发表时间：
2002-11-01
影响因子：
6.7
通讯作者：
Kornecki, E
中科院分区：
文献类型：
--
作者：
Babinska, A;Kedees, MH;Kornecki, E
F11受体（F11 R）是一种细胞粘附分子（CAM），是在人血小板表面发现的免疫球蛋白超家族成员，并确定在血小板聚集、分泌、粘附和扩散中发挥作用。相同的分子也存在于内皮细胞（EC）的紧密连接处，其中它被称为JAM，并通过嗜同性相互作用充当CAM。本研究探讨了F11 R/JAM在血小板与内皮细胞相互作用中的作用。我们在这里报告说，洗过的人血小板特异性地粘附到由固定化的重组sF 11 R制成的基质上。此外，血小板粘附于细胞因子-（TNF-α，INF-γ）刺激的人脐静脉内皮细胞（HUVEC），并且大约40-60%的粘附力由血小板的F11 R和EC之间的嗜同性相互作用施加。这通过F11 R的重组可溶形式、具有N-末端区域的氨基酸序列的两种F11 R肽和F11 R的I-st IG折叠分别抑制血小板粘附到内皮细胞来证明。这项研究表明，F11 R在血小板粘附到姜黄素发炎的内皮细胞，从而在血栓形成和动脉粥样硬化诱导的非裸露的血管炎症过程中的作用。阻断F11 R介导的血小板与EC粘附的药物可能在控制血栓形成、预防心脏病发作和中风方面具有治疗价值。
The F11 receptor (F11R) is a cell adhesion molecule (CAM), member of the immunoglobulin superfamily found on the surface of human platelets, and determined to play a role in platelet aggregation, secretion, adhesion and spreading. The same molecule is present also at tight junctions of endothelial cells (EC) where it is known as JAM and acts as a CAM through homophilic interactions. The role of F11R/JAM in the interaction of platelets with endothelial cells was investigated in the current studies. We report here that washed human platelets adhere specifically to a matrix made of immobilized, recombinant sF11R. Furthermore, platelets adhere to cytokine- (TNF-alpha, INF-gamma) stimulated human umbilical vein endothelial cells (HUVEC), and approximately 40-60% of the adhesive force is exerted by homophilic interactions between the F11R of platelets and EC. This is evidenced by the inhibition of platelet adhesion to endothelial cells by recombinant soluble form of the F11R, and by two F11R peptides with amino acid sequences of the N-terminal region, and in the I-st Ig fold of the F11R, respectively. This study suggests a role for F11R in the adhesion of platelets to cytokine-inflamed endothelial cells and thus in thrombosis and atherosclerosis induced in non-denuded blood vessels by inflammatory processes. Agents that block the F11R-mediated adhesion of platelets to EC may be of therapeutic value in controlling thrombosis, and preventing heart attacks and stroke.