MiR-625-5p suppresses inflammatory responses by targeting AKT2 in human bronchial epithelial cells

Abstract

Asthma is a common chronic inflammatory airway disease; however, whether microRNAs (miRs) could be used in the treatment of asthma remains unclear. The aim of the present study was to investigate the role of miR-625-5p in the inflammatory response of human bronchial epithelial cells (HBECs). Inflammation in the HBEC line, 16HBEC, was induced using different concentrations of lipopolysaccharide (LPS), which demonstrated that 1 µg/ml LPS was an appropriate concentration for further experiments. The association between protein kinase B2 (AKT2) and miR-625-5p was verified using a luciferase reporter assay. LPS was added to 16HBECs following the administration of miR-625-5p mimics or miR-625-5p inhibitors, and cells with silenced or overexpressed AKT2 levels. miR-625-5p was expressed at a high level in LPS-activated 16HBECs. Overexpression of miR-625-5p inhibited interleukin (IL)-6 and tumor necrosis factor (TNF)-α secretion in 16HBECs. Inhibition of miR-625-5p enhanced LPS-induced IL-6 and TNF-α secretion. miR-625-5p negatively regulated the expression of AKT2 in 16HBECs. A dual-luciferase reporter assay system confirmed that miR-625-5p directly targeted the 3'untrans-lated region of AKT2. Transfection with a small interfering RNA against AKT2 inhibited inhibitor of κB phosphorylation. In brief, miR-625-5p may protect LPS-induced HBECs by targeting AKT2 and inhibiting the nuclear factor-κB signaling pathway. Therefore, miR-625-5p may function as an inhibitor of asthma airway inflammation in HBECs by targeting AKT2.