Reticulon 4B (Nogo-B) is necessary for macrophage infiltration and tissue repair
Reticulon 4B (Nogo-B) is necessary for macrophage infiltration and tissue repair
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DOI：
10.1073/pnas.0907359106
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发表时间：
2009-10-13
影响因子：
11.1
通讯作者：
Sessa, William C.
中科院分区：
文献类型：
--
作者：
Yu, Jun;Fernandez-Hernando, Carlos;Sessa, William C.
缺血和伤口愈合过程中的血管形成需要炎症反应与调节血管组装的基因协调。在这里，我们发现网状细胞家族成员4B，又名Nogo-B，在缺血反应中上调，是缺血和伤口愈合后血流恢复所必需的。缺乏Nogo-B的小鼠表现出动脉生成和血管生成减少，这与体内巨噬细胞浸润和炎症基因表达减少有关。从Nogo敲除小鼠中分离的骨髓源性巨噬细胞由于Rac激活受损而减少了扩散和趋化性。骨髓重建实验表明，骨髓细胞中的Nogo对促进巨噬细胞归巢和肢体缺血后功能恢复是必要的。因此，内源性Nogo协调巨噬细胞介导的炎症与动脉发生、伤口愈合和血流控制。
Blood vessel formation during ischemia and wound healing requires coordination of the inflammatory response with genes that regulate blood vessel assembly. Here we show that the reticulon family member 4B, aka Nogo-B, is upregulated in response to ischemia and is necessary for blood flow recovery secondary to ischemia and wound healing. Mice lacking Nogo-B exhibit reduced arteriogenesis and angiogenesis that are linked to a decrease in macrophage infiltration and inflammatory gene expression in vivo. Bone marrow-derived macrophages isolated from Nogo knock-out mice have reduced spreading and chemotaxis due to impaired Rac activation. Bone marrow reconstitution experiments show that Nogo in myeloid cells is necessary to promote macrophage homing and functional recovery after limb ischemia. Thus, endogenous Nogo coordinates macrophage-mediated inflammation with arteriogenesis, wound healing, and blood flow control.