| First Author | Han X | Year | 2016 |
| Journal | FEBS Lett | Volume | 590 |
| Issue | 1 | Pages | 53-67 |
| PubMed ID | 26762170 | Mgi Jnum | J:229918 |
| Mgi Id | MGI:5754896 | Doi | 10.1002/1873-3468.12040 |
| Citation | Han X, et al. (2016) Counter-regulatory paracrine actions of FGF-23 and 1,25(OH)2 D in macrophages. FEBS Lett 590(1):53-67 |
| abstractText | 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-gamma-induced proinflammatory M1 macrophages and Hyp mouse-derived peritoneal macrophages, but not in IL-4-induced M2 anti-inflammatory macrophages. NF-capital KA, CyrillicB and JAK/STAT1 pathways mediated the increased transcription of FGF-23 in response to M1 polarization. FGF-23 stimulated TNF-alpha, 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-alpha. FGF-23 has proinflammatory paracrine functions and counter-regulatory actions to 1,25(OH)2 D on innate immune responses. |
