The role of miR-155 in angiotensin II-induced renal tubular epithelial-mesenchymal transition and its mechanism
SHI Zhewei1, LIU Shengxin1, QIN Chengfan2, ZHANG Liuping3, QIAN Caizhen1
1.Department of Cardiology, Zhuji People’s Hospital of Wenzhou Medical University, Shaoxing 311800, China; 2.The Second Clinical Medical College, Wenzhou Medical University, Wenzhou 325035, China; 3.Department of Cardiology,Zhuji Traditional Chinese Medicine Hospital, Shaoxing 311800, China
SHI Zhewei,LIU Shengxin,QIN Chengfan, et al. The role of miR-155 in angiotensin II-induced renal tubular epithelial-mesenchymal transition and its mechanism[J]. JOURNAL OF WEZHOU MEDICAL UNIVERSITY, 2021, 51(2): 99-104.
Abstract：Objective: To determine the role of miR-155 in angiotensin II-induced epithelial-mesenchymal transition (EMT) of renal tubular epithelial (NRK-52E) cells and to explore its specific regulatory mechanism.Methods: Cultured in vitro, NRK-52E renal tubular epithelial cells were divided as control group, Ang II group,NC miRNA treatment group, miR-155 inhibitor treatment group, solvent control group and Akt agonist treatment group. CCK8 method was used to detect cell proliferation level, and Western blot was used to detect the expression levels of EMT related proteins, TGF-β protein and the phosphorylation level of protein kinase B (AKT). Also, qPCR was used to detect the expression level of miR-155, and the fluorescence intensity of collagen I protein were detected by immunofluorescence staining. Results: With the up-regulation of Ang II concentration, the proliferation ability of NRK-52E cells, TGF-β and the expression levels of EMT-related proteins increased significantly (all P<0.05), and miR-155 expression levels were also significantly up-regulated (P<0.05). Compared with the Ang II treatment group, the expression levels of miR-155, EMT-related proteins and AKT protein phosphorylation levels were significantly reduced in the miR-155 inhibitor treatment group (all P<0.05). Compared with the miR-155 inhibitor treatment group and the solvent control group, the expression levels of EMT-related proteins and the phosphorylation levels of AKT protein in the AKT agonist treatment group were significantly increased (all P<0.05). Conclusion: miR-155 may promote the process of EMT in NRK-52E cells by regulating the AKT pathway.
