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 Lettjournal_title
FEBS lettersauthors
Han X,Li L,Yang J,King G,Xiao Z,Quarles LDdoi
10.1002/1873-3468.12040subject
Has Abstractpub_date
2016-01-01 00:00:00pages
53-67issue
1eissn
0014-5793issn
1873-3468journal_volume
590pub_type
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