中文摘要：

P-selectin glycoprotein ligand-1 (PSGL-1 ) 不仅作为一个锚分子工作由它和 P-selectin 的相互作用在 ischemic 织物捕获单核白血球和另外的白血球到 endothelial 房间，而且 transduces 发信号开始坚挺的粘附。Endothelial 祖先房间从单核白血球被导出并且在 neovascularization 起一个很重要的作用。endothelial 祖先房间的移植是有希望的治疗学的策略改进象心肌、服的梗塞那样的 ischemic 疾病的治疗；然而，它的功效现在被很少移植房间在 ischemic 织物遵守并且积累的事实限制。在这研究，我们试图调查 PSGL-1 基因的 overexpression 是否支持 endothelial 祖先房间粘附活动并且探索内在的机制。我们发现在有人的 PSGL-1 基因的 transfection 以后， endothelial 祖先房间展出了更高的亲密关系到激活的人的脐的静脉 endothelial 房间或重新结合的 P-selectin/ICAM-1 单层。endothelial 祖先房间表面上的 PSGL-1-enhanced 2-integrin 表示的 overexpression，和这效果是 Syk 依赖者。特定的 Syk 禁止者在表面 2-integrin 表示和 endothelial 祖先房间的粘合剂亲密关系上废除了 PSGL-1 的 overexpression 的提高的效果。这些结果建议 Syk 在 endothelial 祖先房间 PSGL-1 下游地在信号 transduction 起一个关键作用，并且 PSGL-1 的 overexpression 通过 Syk 的提高的激活和后面的 integrin 激活改进 endothelial 祖先房间粘合剂性质。

英文摘要：

P-selectin glycoprotein ligand-1 （PSGL-1） not only functions as an anchor molecule to capture monocytes and other leukocytes to endothelial cells in ischemic tissue by its interaction with P-selectin, but also transduces signals to initiate firm adhesion. Endothelial progenitor cells are derived from monocytes and play a very important role in neovascularization. Transplantation of endothelial progenitor cells is a promising therapeutic strategy to improve treatment of ischemic disease such as myocardial and cerebral infarction; however, its efficacy is now limited by the fact that few of the transplanted cells adhere to and accumulate in the ischemic tissue. In this study we aimed to investigate whether the overexpression of PSGL-1 gene promotes endothelial progenitor cells adhesion activity and explore the underlying mechanisms. We found that after transfection with human PSGL-1 gene, endothelial progenitor cells exhibited higher affinity to activated human umbilical vein endothelial cells or recombined P-selectin/ICAM-1 monolayer. The overex- pression of PSGL-1-enhanced β2-integrin expression on endothelial progenitor cells surface, and this effect was Syk dependent. The specific Syk inhibitor abolished the elevating effect of overexpression of PSGL-1 on surface β2-integrin expression and the adhesive affinity of endo- thelial progenitor cells. These results suggested that Syk plays a key role in signal transduction downstream of PSGL-1 in endothelial progenitor cells, and the overexpression of PSGL-1 improves endothelial progenitor cells adhesive properties through enhanced activation of Syk and following integrin activation.