Counter-regulatory paracrine actions of FGF-23 and 1,25(OH)2D in macrophages

被引：102

作者：

Han, Xiaobin ^{[1
]}

Li, Linqiang ^{[1
]}

Yang, Jiancheng ^{[1
]}

King, Gwendalyn ^{[2
]}

Xiao, Zhousheng ^{[1
]}

Quarles, Leigh Darryl ^{[1
]}

机构：

[1] Univ Tennessee, Ctr Hlth Sci, Dept Med, Coleman Bldg,Suite B216,956 Court Ave, Memphis, TN 38163 USA

[2] Univ Alabama Birmingham, Birmingham, AL USA

来源：

FEBS LETTERS | 2016年 / 590卷 / 01期

基金：

美国国家卫生研究院;

关键词：

1; 25(OH)(2)D; FGF-23; interferon gamma; Klotho; lipopolysaccharide; macrophages; FIBROBLAST GROWTH FACTOR-23; CHRONIC KIDNEY-DISEASE; VITAMIN-D; ONCOSTATIN M; KLOTHO; FGF23; EXPRESSION; PHOSPHATE; RECEPTOR; FIBROBLAST-GROWTH-FACTOR-23;

D O I：

10.1002/1873-3468.12040

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Mechanisms underlying the association between fibroblastic growth factor 23 (FGF-23) and inflammation are uncertain. We found that FGF-23 was markedly up-regulated in LPS/INF--induced proinflammatory M1 macrophages and Hyp mouse-derived peritoneal macrophages, but not in IL-4-induced M2 anti-inflammatory macrophages. NF-?B and JAK/STAT1 pathways mediated the increased transcription of FGF-23 in response to M1 polarization. FGF-23 stimulated TNF-, but not IL-6, expression in M0 macrophages and suppressed Arginase-1 expression in M2 macrophages through FGFR-mediated mechanisms. 1,25(OH)(2)D stimulated Arginase-1 expression and inhibited FGF-23 stimulation of TNF-. FGF-23 has proinflammatory paracrine functions and counter-regulatory actions to 1,25(OH)(2)D on innate immune responses.

引用

页码：53 / 67

页数：15

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