PI3 kinase-dependent stimulation of platelet migration by stromal cell-derived factor 1 (SDF-1)
PI3 kinase-dependent stimulation of platelet migration by stromal cell-derived factor 1 (SDF-1)
复制标题
DOI：
10.1007/s00109-010-0680-8
复制
发表时间：
2010-12-01
影响因子：
4.7
通讯作者：
Lindemann, Stephan
中科院分区：
文献类型：
--
作者：
Kraemer, Bjoern F.;Borst, Oliver;Lindemann, Stephan
血小板被认为是静止的细胞，一旦它们粘附到基质上就不会移动。本研究探讨了血小板是否具有迁移能力。与目前的观点相反，我们发现血小板是移动的，能够在表面上迁移，并通过transwell膜和内皮细胞向基质细胞衍生因子1（SDF-1）的来源迁移。SDF-1刺激血小板迁移，导致下游Wiskott-Aldrich综合征蛋白的活化和磷酸化。CXCR 4受体阻断剂AMD 3100、百日咳毒素、用LY 294002或渥曼青霉素抑制磷酸肌醇3-激酶（PI 3激酶）以及用细胞松弛素B破坏肌动蛋白聚合可抑制SDF-1信号传导和随后的血小板迁移。血小板以SDF-1介导的方式迁移的潜力可能重新定义血小板在血管炎症、随后的动脉粥样硬化变性和血管再生的病理生理学中的作用。
Platelets have been regarded as static cells that do not move once they adhere to a matrix. The present study explored, whether platelets are able to migrate. In contrast to the current opinion, we found that platelets were mobile, able to migrate over a surface, and transmigrate through a transwell membrane and endothelium toward a source of stromal cell-derived factor 1 (SDF-1). Platelet migration was stimulated by SDF-1, which led to the downstream activation and phosphorylation of Wiskott-Aldrich syndrome protein. SDF-1 signaling and subsequent platelet migration could be inhibited by CXCR4-receptor blocker AMD3100, pertussis toxin, inhibition of phosphoinositol 3-kinase (PI3 kinase) with LY294002 or wortmannin, and disruption of actin polymerization with cytochalasin B. The potential of platelets to migrate in an SDF-1-mediated fashion may redefine the role of platelets in the pathophysiology of vascular inflammation, subsequent atherosclerotic degeneration, and vascular regeneration.