| First Author | Sun B | Year | 2018 |
| Journal | Cytokine | Volume | 106 |
| Pages | 80-88 | PubMed ID | 29111086 |
| Mgi Jnum | J:318519 | Mgi Id | MGI:6859973 |
| Doi | 10.1016/j.cyto.2017.10.015 | Citation | Sun B, et al. (2018) Role of interleukin 17 in TGF-beta signaling-mediated renal interstitial fibrosis. Cytokine 106:80-88 |
| abstractText | BACKGROUND: Several studies suggest IL-17 is involved in the pathogenesis of organ fibrosis. The exact role of IL-17 in renal interstitial fibrosis has not been fully elucidated. METHODS: We compared the histopathology of renal fibrosis as well as profibrotic TGF-beta signaling in wild-type (WT) and IL-17 knock-out (IL-17(-/-)) mice using UUO as the disease model. To find out the possible mechanisms involved in the exacerbated renal fibrosis happened to IL-17(-/-) mice, we analyzed the pattern of ECM synthesis by different fibroblasts cultured with IL-17 and associated signaling mediators. RESULTS: On day3 and day7, IL-17(-/-) mice developed more severe renal fibrosis compared with WT mice. IL-17 had an inhibitory factor in TGF-beta-induced renal fibroblast activation and ECM synthesis, and sequentially in renal interstitial fibrosis, via down-regulation of Smad -independent pathway (p38MAPK and AKT phosphorylations). CONCLUSION: IL-17 acts an inhibitory factor in TGF-beta-induced renal fibroblast activation and ECM synthesis, and sequentially in renal interstitial fibrosis, via down-regulation of Smad-independent pathway (p38MAPK and AKT phosphorylations). Clarifying the novel regulatory mechanisms of fibrosis by the cytokine IL-17 may lead to a new therapeutic approach for progressive renal disease and fibrosis. |
