MicroRNA-21-5p antagonizes oxidant-mediated apoptosis in alveolar epithelial type II cells by targeting PDCD4

Acute respiratory distress syndrome (ARDS) is a condition characterized by acute inflammation in the lungs. Apoptosis of alveolar epithelial type II (ATII) cells contributes to the initiation and progression of the disease. miRNAs are tightly regulated and their dysregulation plays an important role in human diseases. One such miRNA, miR-21 is shown to be involved in several different diseases. However, its role in ARDS is still not known. Here, we hypothesize that miR-21-5p inhibits apoptosis in ATII cells and protects against ARDS. In the present study, 50 mu M H2O2 was used to induce ATII cell damage to simulate ARDS in vitro. CCK-8 assay was performed to detect cell proliferation and flow cytometry was used to evaluate cell apoptosis. A dual-luciferase assay was performed to confirm whether miR-21 directly targeted the programmed cell death 4 (PDCD4) mRNA. Here, we found that ATII cell apoptosis increased after treatment with 0.5 mM H2O2. Overexpression of miR-21 or knockdown of PDCD4 promoted ATII cell proliferation and inhibited ATII cell apoptosis after treatment with H2O2. We further confirmed that miR-21 regulates PDCD4 expression by targeting its three prime untranslated region (3'-UTR). Our results suggest that miR-21 potentially antagonizes oxidant-mediated apoptosis in alveolar epithelial type II cells. These findings provide new insights in understanding the process of ARDS and also provide a potential target for the treatment of ARDS.