Chavakis Emmanouil, Aicher Alexandra, Heeschen Christopher, Sasaki Ken-ichiro, Kaiser Ralf, El Makhfi Naual, Urbich Carmen, Peters Thorsten, Scharffetter-Kochanek Karin, Zeiher Andreas M, Chavakis Triantafyllos, Dimmeler Stefanie
Molecular Cardiology, Dept. of Medicine III, University of Frankfurt, 60950 Frankfurt, Germany.
J Exp Med. 2005 Jan 3;201(1):63-72. doi: 10.1084/jem.20041402. Epub 2004 Dec 28.
The mechanisms of homing of endothelial progenitor cells (EPCs) to sites of ischemia are unclear. Here, we demonstrate that ex vivo-expanded EPCs as well as murine hematopoietic Sca-1+/Lin- progenitor cells express beta2-integrins, which mediate the adhesion of EPCs to endothelial cell monolayers and their chemokine-induced transendothelial migration in vitro. In a murine model of hind limb ischemia, Sca-1+/Lin- hematopoietic progenitor cells from beta2-integrin-deficient mice are less capable of homing to sites of ischemia and of improving neovascularization. Preactivation of the beta2-integrins expressed on EPCs by activating antibodies augments the EPC-induced neovascularization in vivo. These results provide evidence for a novel function of beta2-integrins in postnatal vasculogenesis.
内皮祖细胞（EPCs）归巢至缺血部位的机制尚不清楚。在此，我们证明体外扩增的EPCs以及小鼠造血Sca-1+/Lin-祖细胞表达β2整合素，其介导EPCs与内皮细胞单层的粘附以及它们在体外趋化因子诱导的跨内皮迁移。在小鼠后肢缺血模型中，来自β2整合素缺陷小鼠的Sca-1+/Lin-造血祖细胞归巢至缺血部位以及改善新生血管形成的能力较低。通过激活抗体对EPCs上表达的β2整合素进行预激活可增强体内EPCs诱导的新生血管形成。这些结果为β2整合素在出生后血管生成中的新功能提供了证据。
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