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Influence of SOCS-1 on OSM-induced Renal Tubular Epithelial-myofibroblast Transdifferentiation
Liu Qingjuan1, Xing Lingling2, Li Jianying3, Liu Shuxia1, Wang Hui1, Duan Huijun1*
1Department of Pathology, Hebei Medical University, Shijiazhuang 050017, China; 2Department of Nephrology, Second Hospital, Hebei Medical University, Shijiazhuang 050000, China; 3Department of Dermatology, People’s Hospita
Abstract: In order to investigate the effect of suppressor of cytokine signaling-1 on oncostatin M-inducedrenal epithelial-myofibroblast transdifferentiation in human renal tubular epithelial cells， stable transfections of HKC with pCR3.1 vector and pCR3.1/SOCS-1 were perfomed with Lipofectamine 2000， and cells were selected with grneticin. Cells were stimulated with OSM. The protein expressions of CK18， α-SMA， SOCS-1 and p-STAT1 were observed by Western blot. The protein synthesis of Col I and FN in the supernatants of the HKC was detected by enzyme-linked immunoadsorbent assay (ELISA). CK18 and α-SMA mRNA were measured by reverse transcription and polymerase chain reaction (RT-PCR). Compared with control group， the expression levels of α-SMA protein and mRNA and p-STAT1 were significantly increased in HKC with OSM stimulation and there was a higher concentrations of Col I and FN in the supernatants. However， the expression of CK18 protein and mRNA were decreased with OSM stimulation. Overexpression of SOCS-1 inhibited OSM-induced high expression of α-SMA protein and mRNA and activation of STAT1， and reversed the expression of CK18 protein and mRNA. Meanwhile， overexpression of SOCS-1 reduced the concentration of Col I and FN in the supernatants of HKC with OSM stimulation. We conclude that overexpression of SOCS-1 inhibits OSM-induced renal tubular epithelial-myofibroblast transdifferentiation maybe partly through blocking activation of STAT1.
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