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

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.

journal_name

FEBS Lett

journal_title

FEBS letters

authors

Han X,Li L,Yang J,King G,Xiao Z,Quarles LD

doi

10.1002/1873-3468.12040

subject

Has Abstract

pub_date

2016-01-01 00:00:00

pages

53-67

issue

1

eissn

0014-5793

issn

1873-3468

journal_volume

590

pub_type

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