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作 者:赵春燕[1] 刘畅[1] 朱忠立[1] 王晓芬[1] 祝国芸 李福祥[1] ZHAO Chun-yan;LIU Chang;ZHU Zhong-li;WANG Xiao-fen;ZHU Guo-yun;LI Fu-xiang(Department of Critical CareMedicine,Chengdu Militam General Hospital,Chengdu Sichuan 610000 , China)
机构地区:[1]成都军区总医院重症医学科,四川成都610000
出 处:《局解手术学杂志》2017年第11期790-795,共6页Journal of Regional Anatomy and Operative Surgery
摘 要:目的探讨百草枯(PQ)诱导大鼠Ⅱ型肺泡上皮细胞RLE-6TN发生上皮间质转化(EMT)的作用及其分子机制。方法将体外培养的大鼠Ⅱ型肺泡上皮细胞RLE-6TN细胞用20μmol/L的百草枯处理24 h,采用倒置显微镜观察细胞形态学变化;RT-PCR和Western blot法检测细胞中β-catenin、上皮表型标记蛋白E-cadherin及间质表型标记蛋白Vimentin的表达;Transwell侵袭实验检测百草枯处理组与阴性对照组细胞侵袭能力变化。使用β-catenin靶向siRNA抑制其表达后,进一步采用RT-PCR和Western blot检测β-catenin、E-cadherin和Vimentin的表达水平,Transwell法检测细胞侵袭能力变化。结果体外百草枯溶液可显著诱导大鼠Ⅱ型肺泡上皮细胞RLE-6TN上皮间质转化的发生,并伴随着细胞侵袭能力的显著增强。靶向沉默β-catenin基因后,百草枯诱导的上皮间质转化过程被逆转,同时细胞侵袭能力显著减弱。结论百草枯通过调控β-catenin来诱导RLE-6TN细胞上皮间质转化的发生,进而促进肺纤维化的形成。Objective To investigate whether paraquat( PQ) induced rat alveolar type Ⅱ cells( RLE-6 TN) epithelial-mesenchymal transition( EMT) and explore the underlying molecular mechanism. Methods RLE-6 TN cells were treated by 20 μmol/L PQ for 24 hours,the morphology was observed by invert microscope. RT-PCR and Western blot were performed to detect the expression level of β-catenin,EMT related markers E-cadherin and vimentin. Then we performed the Transwell invasion assays to detect the ability of cell invasion. Results The results demonstrated that PQ was able to induce the transition of RLE-6 TN cells from epithelial morphology to fibroblast-like morphology,associated with the acquisition of migratory properties. Furthermore,knockdown of β-catenin by using specific siRNA could reverse PQ triggered EMT process and attenuated cell migration ability. Conclusion PQ promotes RLE-6 TN epithelial-mesenchymal transition by upregulating the expression of Wnt/β-catenin.
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