TAK1 regulates fibrosis of renal tubular epithelial cells by regulating p38 MAPK signaling pathway |
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Authors: | DING Wen-fei SONG Lei LIU Hai-yun QIN Jian-hua CAO Ling GAO Li-chao OU San-tao WU Wei-hua |
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Affiliation: | 1. Department of Nephrology, Affiliated Hospital of Southwest Medical University, Luzhou 646000, China;2. Department of Nephropathy, Jiangxi Provincial People's Hospital, Nanchang 330006, China;3. Department of Laboratory Medicine, Jiangxi Provincial People's Hospital, Nanchang 330006, China |
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Abstract: | AIM:To investigate the effect of transforming growth factor-β (TGF-β) activated kinase 1(TAK1) on renal tubular epithelial fibrosis. METHODS:The renal tubular epithelial cell line HK-2 was used as the research object. After induced by TGF-β1, real-time PCR and Western blot were used to detect the expression of TAK1 in the HK-2 cells. TAK1 shRNA lentivirus was used to infect HK-2 cells, real-time PCR and Western blot were used to determine the interference effect on TAK1 expression in the HK-2 cells with TGF-β1 stimulation. Under the condition of treating with p38 MAPK activator anisomycin, the levels of type I collagen and type Ⅲ collagen in the supernatant, and the protein levels of α-smooth muscle actin (α-SMA), connective tissue growth factor (CTGF) and p-p38MAPKThr 180/Tyr 182 in the HK-2 cells with TAK1 knock-down were determined by ELISA and Western blot, respectively. RESULTS:TGF-β1 significantly increased the expression of TAK1 in the HK-2 cells(P<0.05). TAK1 shRNA significantly decreased the expression of TAK1 in the HK-2 cells with TGF-β1 stimulation. Type I collagen and type Ⅲ collagen secreted by the HK-2 cells after treatment with TGF-β1 were increased, the protein levels of α-SMA, CTGF and p-p38MAPKThr 180/Tyr 182 were also increased(P<0.05). Knock-down of TAK1 expression significantly inhibited the secretion of type I and type Ⅲ collagen, reduced the protein levels of α-SMA, CTGF and p-p38MAPKThr 180/Tyr 182 in the TGF-β1-induced HK-2 cells(P<0.05). Treatment with p38 MAPK activator reversed the inhibitory effect of TAK1 knock-down on the secretion of type I and type Ⅲ collagens, and the protein levels of α-SMA, CTGF and p-p38 MAPKThr 180/Tyr 182 in the HK-2 cells(P<0.05). CONCLUSION:Knock-down of TAK1 expression attenuates the TGF-β1 induced fibrosis of renal tubular epithelial cells by inhibiting p38 MAPK signaling pathway. |
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Keywords: | Renal tubular epithelial cells Transforming growth factor-&beta activated kinase 1 p38 MAPK signaling pathway Fibrosis |
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