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

Xiaobin Han, Linqiang Li, Jiancheng Yang, Gwendalyn King, Zhousheng Xiao, Leigh Darryl Quarles

Research output: Contribution to journalArticlepeer-review

80 Scopus citations


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-ΚB 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)2D 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)2D on innate immune responses.

Original languageEnglish (US)
Pages (from-to)53-67
Number of pages15
JournalFEBS Letters
Issue number1
StatePublished - Jan 2016
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology


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