4.7 Article

CTRP6 inhibits cell proliferation and ECM expression in rat mesangial cells cultured under TGF-β1

Journal

BIOMEDICINE & PHARMACOTHERAPY
Volume 97, Issue -, Pages 280-285

Publisher

ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2017.10.091

Keywords

C1q/tumor necrosis factor-related protein 6 (CTRP6); Renal fibrosis; TGF-beta 1; Extracellular matrix (ECM)

Funding

  1. Scientific and Technological Project of Henan Province in China [201003089]

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C1q/tumor necrosis factor-related protein 6 (CTRP6), a member of CTRPs family, was involved in fibrosis. However, the biological function of CTRP6 in renal fibrosis remains elusive. This study aimed to examine the role of CTRP6 in renal fibrosis and explore the possible mechanism. Our results demonstrated that the expression of CTRP6 was significantly downregulated in renal fibrotic tissues and TGF-beta 1-treated NRK-49F cells. In addition, overexpression of CTRP6 inhibited the proliferation, migration, and ECM expression in TGF-beta 1-treated NRK-49F cells. Furthermore, overexpression of CTRP6 attenuated TGF-beta-induced phosphorylation of ERK1/2 in NRK-49F cells. The ERK1/2 inhibitor U0126 enhanced the inhibitory effects of CTRP6 overexpression on cell proliferation, migration and ECM expression in TGF-beta 1-stimulated NRK-49F cells. In conclusion, we have demonstrated that CTRP6 suppressed ECM expression in renal fibroblasts induced by TGF-beta 1 through the ERK signaling pathway. Therefore, CTRP6 may be a potential therapeutic target for the treatment of renal fibrosis.

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