miR-30e-5p Regulates Autophagy and Apoptosis by Targeting Beclin1 Involved in Contrast-induced Acute Kidney Injury

(E-pub Ahead of Print)

Author(s): Xiaoqin Liu, Qingzhao Li, Lixin Sun, Limei Chen, Yue Li, Beibei Huang, Yunshuang Liu, Chunyang Jiang*

Journal Name: Current Medicinal Chemistry


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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.

Keywords: Acute kidney injury, contrast, miR-30e-5p, autophagy, apoptosis, HK-2 cells.

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(E-pub Ahead of Print)
DOI: 10.2174/0929867328666210526125023

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