Department of Nephrology, Huaihe Hospital of Henan University, Kaifeng 475000, Henan Province, China.
Department of Nephrology, Huaihe Hospital of Henan University, Kaifeng 475000, Henan Province, China.
Biomed Pharmacother. 2018 Jan;97:280-285. doi: 10.1016/j.biopha.2017.10.091. Epub 2017 Nov 6.
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-β1-treated NRK-49F cells. In addition, overexpression of CTRP6 inhibited the proliferation, migration, and ECM expression in TGF-β1-treated NRK-49F cells. Furthermore, overexpression of CTRP6 attenuated TGF-β-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-β1-stimulated NRK-49F cells. In conclusion, we have demonstrated that CTRP6 suppressed ECM expression in renal fibroblasts induced by TGF-β1 through the ERK signaling pathway. Therefore, CTRP6 may be a potential therapeutic target for the treatment of renal fibrosis.
C1q/肿瘤坏死因子相关蛋白 6（CTRP6）是 CTRP 家族的一员，参与纤维化。然而，CTRP6 在肾纤维化中的生物学功能仍不清楚。本研究旨在探讨 CTRP6 在肾纤维化中的作用及其可能的机制。
我们的结果表明，CTRP6 在肾纤维化组织和 TGF-β1 处理的 NRK-49F 细胞中的表达明显下调。此外，CTRP6 的过表达抑制了 TGF-β1 处理的 NRK-49F 细胞的增殖、迁移和 ECM 表达。此外，过表达 CTRP6 可减轻 TGF-β1 诱导的 NRK-49F 细胞中 ERK1/2 的磷酸化。ERK1/2 抑制剂 U0126 增强了 CTRP6 过表达对 TGF-β1 刺激的 NRK-49F 细胞中细胞增殖、迁移和 ECM 表达的抑制作用。
总之，我们已经证明，CTRP6 通过 ERK 信号通路抑制 TGF-β1 诱导的肾成纤维细胞中 ECM 的表达。因此，CTRP6 可能是治疗肾纤维化的潜在治疗靶点。
