miR-21 attenuates contrast-induced renal cell apoptosis by targeting PDCD4

被引:19
|
作者
Wang, Kun [1 ]
Bei, Wei-Jie [1 ]
Liu, Yuan-Hui [1 ]
Li, Hua-Long [1 ]
Chen, Shi-Qun [1 ]
Lin, Kai-Yang [1 ]
Zhou, Zhi-Ling [1 ]
Chen, Ji-Yan [1 ,2 ]
Liu, Yong [1 ,2 ]
Tan, Ning [1 ,2 ]
机构
[1] Guangdong Gen Hosp, Guangdong Acad Med Sci, Guangdong Key Lab Coronary Dis, Guangdong Cardiovasc Inst,Dept Cardiol, 106 Zhongshan Second Rd, Guangzhou 510515, Guangdong, Peoples R China
[2] South China Univ Technol, Sch Med, Guangzhou 510100, Guangdong, Peoples R China
基金
中国国家自然科学基金; 美国国家科学基金会;
关键词
microRNA-21; programmed cell death protein 4; contrast medium; contrast-induced acute kidney injury; HK-2; cells; ACUTE KIDNEY INJURY; INDUCED NEPHROPATHY; UP-REGULATION; MICRORNAS; IDENTIFICATION; BIOMARKERS; PATHOGENESIS; CONTRIBUTES; EXPRESSION; PREVENTION;
D O I
10.3892/mmr.2017.7426
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Contrast medium (CM) is widely used in cardiac catheterization; however, it may induce acute kidney injury or renal failure, although the underlying mechanism remains to be elucidated. MicroRNA-21 (miR-21) is involved in renal disease and has been indicated to regulate cellular apoptosis and fibrosis, although its role in CM-induced renal cell injury is unknown. The present study examined the expression and potential targets of miR-21 in human renal proximal tubular epithelial (HK-2) cells following CM treatment. CM induced renal cell apoptosis and decreased miR-21 expression. The expression level of the apoptosis regulator protein, B-cell lymphoma 2 (Bcl-2) was upregulated, whereas that of the apoptosis regulator, Bcl-2-associated X protein (Bax) was downregulated upon transfection of miR-21 mimics; miR-21 overexpression additionally directly inhibited the expression of programmed cell death protein 4 (PDCD4), as determined by a dual luciferase reporter assay, and PDCD4 silencing reduced the rate of HK-2 cell apoptosis. The results of the present study indicated that miR-21 protected renal cells against CM-induced apoptosis by regulating PDCD4 expression.
引用
收藏
页码:6757 / 6763
页数:7
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