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FEBS Lett. 2016 Jan;590(1):53-67. doi: 10.1002/1873-3468.12040. Epub 2016 Jan 9.

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

Author information

1
Department of Medicine, University of Tennessee Health Science Center, Memphis, TN, USA.
2
University of Alabama in Birmingham, AL, USA.

Abstract

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-γ-induced proinflammatory M1 macrophages and Hyp mouse-derived peritoneal macrophages, but not in IL-4-induced M2 anti-inflammatory macrophages. NF-КB and JAK/STAT1 pathways mediated the increased transcription of FGF-23 in response to M1 polarization. FGF-23 stimulated TNF-α, 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-α. FGF-23 has proinflammatory paracrine functions and counter-regulatory actions to 1,25(OH)2 D on innate immune responses.

KEYWORDS:

1,25(OH)2D; FGF-23; Klotho; interferon gamma; lipopolysaccharide; macrophages

PMID:
26762170
PMCID:
PMC5079529
DOI:
10.1002/1873-3468.12040
[Indexed for MEDLINE]
Free PMC Article

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