摘要
目的:研究上调大鼠肾小管上皮细胞中trip-1蛋白的表达量对TGF-β1诱导的上皮细胞转分化的影响。方法:包装人TRIP-1基因重组腺病毒,用其感染NRK52E细胞36 h上调内源性trip-1蛋白表达量,之后用10 ng/ml的TGF-β1对细胞进行刺激诱导,72 h后做Western Blot检测细胞中E-cadherin蛋白和α-SMA蛋白表达量。结果:①包装的人TRIP-1基因重组腺病毒感染细胞能够有效上调细胞中trip-1蛋白的表达量。②上调细胞中trip-1蛋白表达量,对TGF-β1引起的NRK52E细胞中E-cadherin蛋白表达水平降低有所抑制,但对TGF-β1引起的NRK52E细胞中α-SMA蛋白表达水平升高没有明显调节作用。结论:上调大鼠肾小管上皮细胞中trip-1蛋白的表达量在一定程度上抑制了TGF-β1诱导的NRK52E细胞转分化。
Objective： To investigate the effect of over-expression of trip-1 protein on TGF-β1-induced epithelial-mesenchymal transition in NRK52E cells. Methods： Produce recombinant adenoviruses with human TRIP-1 gene, which was used to infect NRK52E cells to up regulate the expression of trip- 1 protein, then NRK52E cells were stimulated with 10 ng/ml TGF-β1, and the expression levels of E-cadherin protein and α-SMA protein in NRK52E cells were determined by Western Blot Assay after 72 h. Results： ①The recombinant adenoviruses with human TRIP-1 gene could up regulate the expression of trip-1 protein in NRK52E cells effectively. ②Over-exo pression of trip-1 protein could inhibit TGF-β1-induced down-regulation of E-cadherin protein expression in NRK52E cells, but had little effect on TGF-β1-induced up-regulation of a-SMA protein expression. Conclusion： Over-expression of trip-1 protein could partly inhibit TGF-β1-induced epithelial-mesenchymal transition in NRK52E cells.
出处
《现代生物医学进展》
CAS
2013年第7期1201-1204,共4页
Progress in Modern Biomedicine
基金
深圳市科技局基础项目(JC200903180532A)
教育部博士点基金项目(20090002120055)
