Long non-coding RNA SNHG5 suppresses the development of acute respiratory distress syndrome by targeting miR-205/COMMD1 axis.

Abstract

Previous studies have reported the important roles of long non-coding RNAs (lncRNAs) in acute respiratory distress syndrome (ARDS). Here, we focus on the role and regulatory mechanism of lncRNA SNHG5 in ARDS. LPS was used to induce mice to establish ARDS model in vivo and to induce A549 cells to establish ARDS model in vitro. qRT-PCR was performed to determine the expressions of SNHG5, miR-205, and inflammatory cytokines. MTT assay was applied to detect cell viability. Dual-luciferase reporter (DLR) assay was performed to test the interactions among SNHG5, miR-205 and COMMD1. Western blot was used to detect the protein expression of COMMD1. Lung injury was evaluated by evaluating the score of lung injury, lung wet/dry weight ratio, and myeloperoxidase (MPO) activity. SNHG5 was downregulated, while miR-205 was upregulated in the serum of ARDS patients and lung tissues of LPS-induced mice. Upregulation of SNHG5 or down-regulation of miR-205 inhibited inflammation and promoted the viability of LPS-induced A549 cells. SNHG5 alleviated the lung injury of ARDS mice. MiR-205 was a target of SNHG5 and inversely correlated with SNHG5. COMMD1 was targeted by miR-205, and was positively regulated by SNHG5. MiR-205 mimics or sh-COMMD1 reversed the promoting effect of SNHG5 on cell viability and the suppressing effect of SNHG5 on inflammation in cellular model of ARDS. Meantime, miR-205 mimics reversed the relieving effect of SNHG5 on lung injury in mouse model of ARDS. SNHG5 acted as a sponge for miR-205 to ameliorate LPS-induced ARDS by regulating COMMD1.