MicroRNA-503 regulates high-glucose induced apoptosis of renal tubular epithelial cells by targeting Bcl-2
10.3760/cma.j.issn.1001-7097.2017.06.008
- VernacularTitle:微RNA-503通过靶向调控Bcl-2介导高糖诱导的人肾小管上皮细胞凋亡
- Author:
Xu CAO
;
Jia LIU
;
Qiuling FAN
;
Xu WANG
;
Li XU
;
Xue ZHAO
;
Lining WANG
- Keywords:
MicroRNAs;
Diabetic nephropathies;
Apoptosis;
Bcl-2;
Renal tubular epithelial cells
- From:
Chinese Journal of Nephrology
2017;33(6):447-452
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the expression vibration of microRNA-503(miR-503) and its effect on target gene Bcl-2,caspase enzyme activity and apoptosis of human renal tubular epithelial cells (HK-2) induced by high glucose,and to clarify the pathogenesis of renal tubular injury induced by high glucose.Methods HK-2 cells were cultured in normal glucose group (NG),mannitol hypertonic control group (MA),and high glucose group (HG).The morphology of apoptotic cells was observed using inverted microscope.The expression of miR-503 was determined using realtime quantitative PCR.The apoptosis rate of HK-2 cells was detected by Annexin V-FITC double dye using flow cytometry instrument.The expression of Bcl-2 and cleaved caspase-9 were detected by Western blotting.Results In the high glucose and mannitol groups HK-2 cell,an obviously increased apoptotic rate was observed under inverted microscope compared with normal glucose group (P ＜ 0.05).MA and HG up-regulated miR-503 expression (P ＜ 0.01),down-regulated anti-apoptotic protein Bcl-2 expression (P ＜ 0.05) and up-regulated cleaved caspase-9 (P ＜ 0.05).Conclusions The expression of miR-503 increases in HK-2 cells cultured by high glucose and mannitol.MiR-503 promotes apoptosis of HK-2 cells via activating mitochondrial apoptotic pathways and enhancing cleaved caspase-9 for Bcl-2 insufficiency.The tubular toxicity of high glucose is partly due to osmotic pressure.The miR-503 may be involved in diabetic tubular injury and may be a new therapeutic target of DN.
