Colony-Stimulating Factor-1 Promotes Kidney Growth and Repair via Alteration of Macrophage Responses
Colony-Stimulating Factor-1 Promotes Kidney Growth and Repair via Alteration of Macrophage Responses
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DOI：
10.1016/j.ajpath.2011.05.037
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发表时间：
2011-09-01
影响因子：
6
通讯作者：
Ricardo, Sharon D.
中科院分区：
文献类型：
--
作者：
Alikhan, Maliha A.;Jones, Christina V.;Ricardo, Sharon D.
集落刺激因子(CSF)-1控制巨噬细胞的生存、增殖和分化，巨噬细胞被认为是先天和获得性免疫系统的清道夫和代理商。由于它们的可塑性，巨噬细胞在发育和组织稳态中被赋予了许多其他重要的作用。我们提出的证据表明，CSF-1在出生后器官生长和肾脏修复中起着重要的营养作用。值得注意的是，出生后注射CSF-1增加了肾脏的重量和体积，并与组织巨噬细胞数量增加有关。此外，CSF-1通过招募和影响巨噬细胞进入修复状态，促进小鼠缺血再灌注损伤后的出生后肾脏修复。CSF-1治疗通过小管上皮细胞替代、间质纤维化衰减和功能恢复迅速加速肾修复。对CSF-1处理的肾脏巨噬细胞的分析显示，已知的CSF-1靶点胰岛素样生长因子-1和抗炎基因的表达增加。综上所述，这些数据表明CSF-1在肾脏生长、促进内源性修复和炎症损伤的消退中很重要。[J] .中华病理学杂志，2011,29(1);1243-1256。DOI: 10.1016 / j.ajpath.2011.05.037)
Colony-stimulating factor (CSF)-1 controls the survival, proliferation, and differentiation of macrophages, which are recognized as scavengers and agents of the innate and the acquired immune systems. Because of their plasticity, macrophages are endowed with many other essential roles during development and tissue homeostasis. We present evidence that CSF-1 plays an important trophic role in postnatal organ growth and kidney repair. Notably, the injection of CSF-1 postnatally enhanced kidney weight and volume and was associated with increased numbers of tissue macrophages. Moreover, CSF-1 promotes postnatal renal repair in mice after ischemia-reperfusion injury by recruiting and influencing macrophages toward a reparative state. CSF-1 treatment rapidly accelerated renal repair with tubular epithelial cell replacement, attenuation of interstitial fibrosis, and functional recovery. Analysis of macrophages from CSF-1-treated kidneys showed increased expression of insulin-like growth factor-1 and anti-inflammatory genes that are known CSF-1 targets. Taken together, these data suggest that CSF-1 is important in kidney growth and the promotion of endogenous repair and resolution of inflammatory injury. (Am J Pathol 2011, 179: ;1243-1256. DOI: 10.1016/j.ajpath.2011.05.037)