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.