自噬
连环素
细胞凋亡
转染
化学
流式细胞术
纤维化
转化生长因子
癌症研究
信号转导
细胞
免疫印迹
细胞生物学
细胞生长
Wnt信号通路
分子生物学
生物
医学
病理
生物化学
基因
作者
Zhizhong Zhang,Zhenzi Cao,Bohui Zhang,Xiangming Gao,Bing Fan,Feng Tian,Pengde Kang,Yongxiang Zhao
出处
期刊:PubMed
日期:2023-09-01
卷期号:53 (5): 749-759
摘要
To verify whether miR-150-5p modulates the development of renal fibrosis and its mechanism.Transforming growth factor (TGF)-β1 was implemented on HK-2 cells to construct a renal fibrosis in vitro model. Inhibition of autophagy was performed on HK-2 cells by treating with 3-methyladenine (3-MA, an inhibitor of autophagy). HK-2 cells experienced transfection by miR-150-5p mimics/inhibitor and pcDNA-β-catenin plasmids, and the negative controls. Dual luciferase reporter gene assay was applied to validate the relationship between miR-150-5p and β-catenin. Cell apoptosis exploration was implemented by flow cytometry assay. The level detection of CoII, α-SMA, miR-150-5p and β-catenin was executed by real-time quantitative reverse transcription-polymerase chain reaction. The expression of CoII, α-SMA, LC3I, LC3II, Bax, Cleaved Caspase 3, Beclin 1, Bcl-2 and β-catenin proteins was monitored by western blot.Autophagy was inhibited in TGF-β1-induced HK-2 cells. MiR-150-5p alleviated fibrosis, enhanced autophagy, and inhibited apoptosis in TGF-β1-induced HK-2 cells. β-catenin was a target of miR-150-5p. Autophagy inhibition or β-catenin partially counteracted miR-150-5p effect on TGF-β1-induced fibrosis in HK-2 cells.MiR-150-5p alleviates renal tubular epithelial cell fibrosis by activating autophagy via β-catenin signaling.
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