MicroRNA-29a enhances autophagy in podocytes as a protective mechanism against high glucose-induced apoptosis by targeting heme oxygenase-1

W.-X. Fan, X.-L. Wen, H. Xiao, Q.-P. Yang, Z. Liang

Department of Nephrology, the First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan Province, China. angxie810@163.com

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• Metabolism

OBJECTIVE: To evaluate the effects of miR-29a on the high glucose (HG)-induced apoptosis and the correlation between miR-29a and heme oxygenase-1 (HO-1) and the underlying molecular mechanism.

MATERIALS AND METHODS: The cell apoptosis was analyzed by the flow cytometry, and the cells autophagy was evaluated using the transmission electron microscopy. Luciferase reporter assay was carried out to detect the correlation between miR-29a and HO-1. Besides, reverse transcription-PCR and Western blot were applied to detect the mRNA and protein levels.

RESULTS: The expression of miR-29a was significantly decreased in the HG-treated podocytes. Besides, miR-29a overexpression could promote cellular autophagy and significantly reduce HG-induced podocytes apoptosis. Moreover, HO-1 was a direct target of miR-29a and the pre-autophagy and the anti-apoptotic effects of miR-29a on HG-treated podocytes could be significantly reversed by the HO-1 siRNA administration.

CONCLUSIONS: MiR-29a functionally promoted podocytes autophagy and inhibited apoptosis through the HO-1dependent pathway in the HG condition.

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