miR-30e-5p Regulates Autophagy and Apoptosis by Targeting Beclin1 Involved in Contrast-induced Acute Kidney Injury.
Curr Med Chem
; 28(38): 7974-7984, 2021.
Article
en En
| MEDLINE
| ID: mdl-34042027
ABSTRACT
AIMS:
This study aims to verify if miR-30e-5p targets Beclin1 (BECN1), a key regulator of autophagy, and investigate the function of miR-30e-5p and Beclin1 through mediating autophagy and apoptosis in contrast-induced acute kidney injury (CIAKI).METHODS:
Human renal tubular epithelial HK-2 cells were treated with Urografin to construct a cell model of CI-AKI. Real-time reverse transcription-polymerase chain reaction was used to detect gene expression. The dual-luciferase reporting assay and endogenous validation were used to verify targeting and regulating function. The expressions of protein were detected using Western blot. Cell proliferation was detected using methylthiazolyldiphenyl- tetrazolium bromide (MTT) assay. Cell apoptosis was detected using terminal- deoxynucleoitidyl transferase mediated nick end labeling assay, and autophagy was detected using transmission electron microscopy.RESULTS:
HK-2 cells exposed to Urografin for 2 h induced a significant increase in miR-30e-5p. miR-30e-5p had a targeting effect on Beclin1. Moreover, Urografin exposure can enhance cell apoptosis by increasing caspase 3 gene expression and inhibiting autophagy, which was induced by decreased Beclin1 expression regulated by miR-30e-5p, thereby resulting in renal cell injury. Downregulation of miR-30e-5p or upregulation of Beclin1 restored cell vitality by promoting autophagy and suppressing apoptosis in Urografin-treated cells.CONCLUSION:
Urografin increased the expression of miR-30e-5p in HK-2 cells and thus decreased Beclin1 levels to inhibit autophagy, but induced apoptosis, which may be the mechanism for CI-AKI.Palabras clave
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
MicroARNs
/
Lesión Renal Aguda
/
Beclina-1
Límite:
Humans
Idioma:
En
Revista:
Curr Med Chem
Asunto de la revista:
QUIMICA
Año:
2021
Tipo del documento:
Article
País de afiliación:
China