摘要
为研究细胞因子信号传导抑制蛋白-1(suppressors of cytokine signaling-1,SOCS-1)对白介素-1β(interleukin-1β,IL-1β)诱导的人肾小管上皮细胞转分化的影响,构建了稳定表达SOCS-1的人肾近曲小管上皮细胞(HKC)。用IL-1β(10 ng/mL)刺激48 h后,用Western blot、酶联免疫吸附和RT-PCR方法分析显示:IL-1β刺激使不转染的细胞和转染空载体的细胞中α-平滑肌肌动蛋白(α-smooth muscle actin 1,α-SMA)和磷酸化信号转导及转录激活因子1(phospho-signal transducersand activators of transcription 1,p-STAT1)表达增加,Ⅰ型胶原(collagenⅠ,ColⅠ)和纤维连接蛋白(fibronectin,FN)的分泌增加,而细胞角蛋白18(cytokeratin 18,CK18)的表达减少。SOCS-1过表达能抑制IL-1β刺激引起的α-SMA和p-STAT1的表达,减少ColⅠ和FN的分泌,同时能够部分恢复IL-1β刺激引起的CK18的表达。可见,SOCS-1过表达能抑制IL-1β诱导的肾小管上皮细胞转分化,此过程可能与STAT1的磷酸化受抑有关。
In order to investigate the effect of suppressor of cytokine signaling-1 on renal epithelial- myofibroblast transdifferentiation induced by interleukin-1βin human renal tubular epithelial cells, we constructed stable transfection of HKC with pCR3.1/SOCS-1. The cells were collected after stimulated 48 h with IL-1β （10 ng/mL）. The protein and mRNA were observed by immunocytochemistry, Western blot, enzyme-linked immunoadsorbent assay （ELISA） and reverse transcription and polymerase chain reaction （RT-PCR）. The resultssuggested that after stimulated by IL-1β, the expression levels of a-SMA, p-STAT1, ColI and FN were significantly increased, however, the expression of CK18 decreased in control group and transfected with pCR3.1 vector group. Overexpression of SOCS-1 inhibited IL-1β-induced high expression of a-SMA, STAT1, ColI and FN. Meanwhile, overexpression of SOCS-1 reversed the expression of CK18 in HKC with IL-1β stimulation. We conclude that overexpression of SOCS-1 inhibits IL-1β-induced renal tubular epithelial-myofibroblast transdifferentiation maybe partly through blocking activation of STAT1.
出处
《中国细胞生物学学报》
CAS
CSCD
北大核心
2012年第1期41-48,共8页
Chinese Journal of Cell Biology
基金
河北省自然科学基金(No.C2009001083)
河北省卫生厅医学科学研究重点课题(No.20090056)资助项目~~
