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本文引用的文献

1
Disease-specific, neurosphere-derived cells as models for brain disorders.疾病特异性神经球衍生细胞作为脑疾病模型。
Dis Model Mech. 2010 Nov-Dec;3(11-12):785-98. doi: 10.1242/dmm.005447. Epub 2010 Aug 10.
2
An antibody against the colony-stimulating factor 1 receptor depletes the resident subset of monocytes and tissue- and tumor-associated macrophages but does not inhibit inflammation.一种针对集落刺激因子 1 受体的抗体耗尽了常驻单核细胞亚群以及组织和肿瘤相关巨噬细胞,但不抑制炎症。
Blood. 2010 Nov 11;116(19):3955-63. doi: 10.1182/blood-2010-02-266296. Epub 2010 Aug 3.
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CSF-1, IGF-1, and the control of postnatal growth and development.CSF-1、IGF-1 与出生后生长发育的调控。
J Leukoc Biol. 2010 Sep;88(3):475-81. doi: 10.1189/jlb.0310158. Epub 2010 Jun 2.
4
Macrophage Wnt7b is critical for kidney repair and regeneration.巨噬细胞 Wnt7b 对于肾脏修复和再生至关重要。
Proc Natl Acad Sci U S A. 2010 Mar 2;107(9):4194-9. doi: 10.1073/pnas.0912228107. Epub 2010 Feb 16.
5
CSF-1 signals directly to renal tubular epithelial cells to mediate repair in mice.集落刺激因子-1直接向肾小管上皮细胞发出信号,以介导小鼠的修复过程。
J Clin Invest. 2009 Aug;119(8):2330-42. doi: 10.1172/JCI39087. Epub 2009 Jul 1.
6
Trophic macrophages in development and disease.发育和疾病中的营养性巨噬细胞。
Nat Rev Immunol. 2009 Apr;9(4):259-70. doi: 10.1038/nri2528.
7
Alternative activation of macrophages: an immunologic functional perspective.巨噬细胞的替代性激活:免疫学功能视角
Annu Rev Immunol. 2009;27:451-83. doi: 10.1146/annurev.immunol.021908.132532.
8
Exploring the full spectrum of macrophage activation.探索巨噬细胞激活的全谱。
Nat Rev Immunol. 2008 Dec;8(12):958-69. doi: 10.1038/nri2448.
9
The isolation and characterization of murine macrophages.小鼠巨噬细胞的分离与鉴定
Curr Protoc Immunol. 2008 Nov;Chapter 14:14.1.1-14.1.14. doi: 10.1002/0471142735.im1401s83.
10
Macrophage diversity in renal injury and repair.肾损伤与修复中的巨噬细胞多样性
J Clin Invest. 2008 Nov;118(11):3522-30. doi: 10.1172/JCI36150.

集落刺激因子-1 通过改变巨噬细胞反应促进肾脏生长和修复。

Colony-stimulating factor-1 promotes kidney growth and repair via alteration of macrophage responses.

机构信息

Monash Immunology and Stem Cell Laboratories (MISCL), Monash University, Melbourne, Australia.

出版信息

Am J Pathol. 2011 Sep;179(3):1243-56. doi: 10.1016/j.ajpath.2011.05.037. Epub 2011 Jul 14.

DOI:10.1016/j.ajpath.2011.05.037
PMID:21762674
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3157188/
Abstract

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.

摘要

集落刺激因子(CSF-1)控制巨噬细胞的存活、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效应细胞。由于其可塑性,巨噬细胞在发育和组织稳态中具有许多其他重要作用。我们提供的证据表明,CSF-1 在出生后器官生长和肾脏修复中发挥重要的营养作用。值得注意的是,CSF-1 在出生后注射可增强肾脏重量和体积,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向修复状态促进缺血再灌注损伤后的出生后肾脏修复。CSF-1 治疗可迅速加速肾脏修复,包括肾小管上皮细胞替代、间质纤维化减轻和功能恢复。对 CSF-1 治疗肾脏中的巨噬细胞进行分析显示,胰岛素样生长因子-1 和抗炎基因的表达增加,这些基因是 CSF-1 的已知靶标。总之,这些数据表明 CSF-1 在肾脏生长以及促进内源性修复和炎症损伤消退方面具有重要作用。