摘要
目的探讨TGF-β1介导的Smad通路在肾脏纤维化中的作用及机制。方法不同浓度的TGF-β1刺激肾小管上皮细胞48 h,分别光镜、Western Blot、细胞免疫荧光观察肾脏纤维化相关指标变化,以及Smad通路蛋白表达情况等。结果光镜下TGF-β1浓度为10 ng/ml时,可明显诱导肾小管上皮细胞纤维化,并且Western Blot、细胞免疫荧光显示其α-SMA表达量增加,E-cadherin表达量减少;Smad通路中,p-Smad2、p-Smad3表达量增加。肾脏纤维化的细胞模型中,Zeb1、Snail的表达量增加,miR-200c的表达量降低。结论一定浓度的TGF-β1可诱导肾小管上皮细胞纤维化,其主要通过激活下游的Smad通路,可能与Zeb1、Snail的表达量增加、miR-200c的表达量降低有关。
Objective To clarify the role of TGF-β1-mediated Smad pathway in renal fibrosis.Methods different concentrations of TGF-β1 stimulate renal tubular epithelial cells 48 hours,light microscopy,Western Blot,cell immunofluorescence observation of renal fibrosis Changes in indicators,and Smad pathway protein expression. Results The expression of α-SMA was increased and the expression of E-cadherin was decreased by Western Blot and immunofluorescence at the time of TGF-β1 concentration of 10 ng/ml,which could significantly induce fibrosis of renal tubular epithelial cells. p-Smad2,p-Smad3 expression increased in the Smad pathway. In addition,the expression of Zeb1,Snail was increased in the cell model of renal fibrosis.Conclusion A certain concentration of TGF-β1 can induce renal tubular epithelial fibrosis,which mainly through the activation of the downstream Smad pathway may be related to the increased expression of Zeb1,Snail,and the decreased expression of miR-200 c.
作者
赵亚亚
钟成
李悦
宋伟伟
赵卫红
ZHAO Yaya;ZHONG Cheng;LI Yue;SONG Weiwei;ZHAO Weihong(Division of Nephrology,Department of Geriatric,the First Affiliated Hospital of Nanjing Medical University,Nanjing 210029,China)
出处
《解放军预防医学杂志》
CAS
2018年第4期427-430,458,共5页
Journal of Preventive Medicine of Chinese People's Liberation Army
基金
国家重点基础研究发展计划(No.2013CB530803)
国家自然科学基金资助项目(No.H0511-81370843
81670677)
中华医学会临床医学科研专项资金(No.15020020590)
