MiR-26a protects type II alveolar epithelial cells against mitochondrial apoptosis

B.-Y. Xu, Y.-L. Li, B. Luan, Y.-L. Zhang, T.-M. Jia, J.-Y. Qiao

Department of Pediatrics Medicine, The Third Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China. qaksqo@163.com

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• Respiratory Medicine

OBJECTIVE: This study aims to investigate the miR-26a effects on H2O2-induced apoptosis of Type II alveolar epithelial cells (AEC-II) and the potential mechanism.

MATERIALS AND METHODS: AEC-II cells were treated with 0.5 mmol/L H2O2 to mimic cellular model of acute lung injury. Transmitting electron microscopy (TEM) was employed to observe the change of morphological structures. After infecting with miR-26a mimics, flow cytometry was performed to detect cell apoptosis. Western blot was also done to explore mitochondrial apoptosis-related markers: Caspase-3, B-cell lymphoma-2 (Bcl-2) and Bax. AEC-II cells treated with 0.5 mmol/L H2O2 exhibited significant cell apoptosis. Overexpression using miR-26a mimics partially reversed the effects of H2O2-induced apoptosis in AEC-II cells, evidenced by flow cytometry results.

RESULTS: Further Western blot results revealed increased levels of Caspase-3 and Bax, and the decreased Bcl-2 level after infecting with miR-26a mimics, indicating miR-26a has protective effects against mitochondrial apoptosis in AEC-II cells.

CONCLUSIONS: MiR-26a protected AEC-II cells against apoptosis via mitochondrial pathway. Thus, miR-26a promises to be a potential therapy in treatment of Acute Respiratory Distress Syndrome (ARDS).

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