Influence of miR-142-3p on Pulmonary Fibrosis Through Regulation of p53/NF-κB

ObjectivesTo investigate the role of miR-142-3p in the bleomycin-induced idiopathic pulmonary fibrosis (IPF) mouse model and elucidate its targets. MethodsIn vitro model: Alveolar epithelial cells (AECs) were isolated and treated with bleomycin (50 & mu;g/mL) or PBS for 12 h. In vivo model: Bleomycin (5 mg/kg) was injected into the trachea under anesthesia and aseptic conditions, and controls were treated with equal saline. After the completion of modeling, proteins and RNA were extracted. p53/NF-& kappa;B signaling factors were evaluated by western blot or immunohistochemistry. IL-1 & beta; and MMP-9 levels were measured by ELISA. The lentiviral transfection technique was used to overexpress miR-142-3p. ResultsIn IPF, miR-142-3p was identified to play a negative regulatory role in lung epithelial cell senescence. Bleomycin treatment significantly reduced miR-142-3p expression in a concentration-dependent manner in vitro. miR-142-3p overexpression inhibited bleomycin-induced cellular senescence in vivo. In particular, miR-142-3p negatively regulated collagen deposition in pulmonary fibrosis by regulating p53/NF-& kappa;B expression. ConclusionMiR-142-3p plays an important role in the development of IPF by negatively regulating the p53/NF-& kappa;B network.