Medizinische Klinik III, Kardiologie und Kreislauferkrankungen, Eberhard Karls Universität, Tübingen, Germany.
J Thromb Haemost. 2013 Nov;11(11):1954-67. doi: 10.1111/jth.12404.
Platelets are a major source of CXCL12 (stromal cell-derived factor -1α, SDF-1α) and store CXCL12 as part of their α-granule secretome. Platelet activation enhances surface expression and release of CXCL12. Platelets and megakaryocytes express CXCR4, the major receptor for CXCL12, and interaction of CXCL12 with CXCR4 regulates megakaryopoiesis and the function of circulating platelets. Platelet-derived CXCL12 also modulates paracrine mechanisms such as chemotaxis, adhesion, proliferation and differentiation of nucleated cells, including progenitor cells. Platelet-derived CXCL12 enhances peripheral recruitment of progenitor cells to the sites of vascular and tissue injury both in vitro and in vivo and thereby promotes repair mechanisms. CXCL12 expression on platelets is elevated in patients with acute myocardial infarction, correlates with the number of circulating progenitor cells, is associated with preservation of myocardial function and is an independent predictor of clinical outcome. Administration of recombinant CXCL12 reduces infarct size following transient ischemia in mice. The present review summarizes the role of platelet-derived CXCL12 in cardiovascular biology and its diagnostic and therapeutic implications.
血小板是 CXCL12（基质细胞衍生因子-1α，SDF-1α）的主要来源，并将 CXCL12 作为其 α 颗粒分泌组的一部分储存。血小板激活增强了 CXCL12 的表面表达和释放。血小板和巨核细胞表达 CXCR4，这是 CXCL12 的主要受体，CXCL12 与 CXCR4 的相互作用调节巨核细胞生成和循环血小板的功能。血小板衍生的 CXCL12 还调节旁分泌机制，如趋化性、黏附、增殖和核细胞（包括祖细胞）的分化。血小板衍生的 CXCL12 增强了祖细胞在外周向血管和组织损伤部位的募集，无论是在体外还是体内，从而促进了修复机制。急性心肌梗死患者的血小板上 CXCL12 表达升高，与循环祖细胞的数量相关，与心肌功能的保存相关，是临床结果的独立预测因子。重组 CXCL12 的给药可减少小鼠短暂缺血后的梗死面积。本综述总结了血小板衍生的 CXCL12 在心血管生物学中的作用及其诊断和治疗意义。
