MiRNA-148b targeted AMPKα1 mediates high glucose-induced apoptosis in human renal tubular epithelial cells via oxidative stress
10.3760/cma.j.issn.1001-7097.2019.01.007
- VernacularTitle:miRNA-148b靶向AMPKα1通过氧化应激介导高糖诱导的人肾小管上皮细胞凋亡
- Author:
Ying YANG
1
;
Qiuling FAN
;
Lulu LI
;
Xu WANG
;
Si WEN
;
Li XU
Author Information
1. 中国医科大学附属第一医院肾内科
- Keywords:
Diabetic nephropathy;
Oxidative stress;
Renal tubular epithelial cells;
MiRNA-148b;
AMPKα1
- From:
Chinese Journal of Nephrology
2019;35(1):43-47
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the expression and mechanism of microRNA-148b (miRNA-148b) in high glucose-induced renal tubular injury.Method HK-2 cells cultured in vitro were divided into normal glucose group,mannitol hypertonic control group and high glucose group.After 48 hours of culture,the expression of miRNA-148b was detected by real-time quantitative PCR.2',7'-Dichlorodihydrofluorescein diacetate (DCFH-DA) was used for detecting production of ROS and observed under fluorescence microscope for analysis;The expression of AMPKot1,Bcl-2,NOX2,NOX4,activated caspase3 (cleaved-caspase3) were detected by Western blotting.Results Compared with the normal glucose group,the expression of miRNA-148b was up-regulated in HK-2 cells in high glucose group and hypertonic group (P ＜ 0.01),and the production of ROS increased (P ＜ 0.01).The expression of NOX2 and NOX4 was increased,AMPKα1 and Bcl-2 decreased,and cleaved caspase-3 was increased (all P ＜ 0.01).Conclusions HG up-regulated miRNA-148b expression and down-regulated its target gene AMPKα1 which promotes the expression of NOX2 and NOX4 in HK-2 cells.MiRNA-148b promotes apoptosis of HK-2 cells via increasing production of ROS and enhancing cleaved-caspase3 for Bcl-2 insufficiency.The tubular toxicity of high glucose is partly due to osmotic pressure.MiRNA-148b may be involved in the pathological injury of diabetic nephropathy and is expected to become a new therapeutic target for diabetic nephropathy.
