MiR‑21‑5p regulates type II alveolar epithelial cell apoptosis in hyperoxic acute lung injury.

Abstract

Hyperoxia-induced acute lung injury (HALI) as one of the most common complications in patents on mechanical ventilation, and there are no efficient methods to overcome this at present. It was hypothesized that microRNA 21-5p(miR-21-5p) can promote the survival of type II alveolar epithelial cells (AECII), alleviating HALI. The present study aimed to combine gene chip analysis with the overexpression miR-21-5p to develop a novel therapeutic option for HALI. It was found that AECII apoptosis was an important pathogenic event in the development of HALI, and the overexpression of miR-21-5p prevented HALI, associated with reducing AECII apoptosis. These results were obtained using adenoviral/lentiviral vectors, which overexpressed miR-21-5p, to transfect AECII cells in vitro and in vivo. It was found that the overexpression of miR-21-5p reduced the apoptotic rate of the AECII cells. In addition, miR-21-5p decreased the ratio of B-cell lymphoma 2 (Bcl-2)-associated X protein/Bcl-2 and the expression of caspase-3. It was also revealed that the overexpression of miR-21-5p alleviated acute lung injury in adult rats exposed to a hyperoxic environment. These results suggest that miR-21-5p may become a novel therapeutic option for patients with HALI, by protecting AECII cells from apoptosis.