Long non-coding RNA NEAT1/miR-193a-3p regulates LPS-induced apoptosis and inflammatory injury in WI-38 cells through TLR4/NF-κB signaling.

Pneumonia is a primary pulmonary infection disease with a high morbidity and mortality worldwide. Identification of key long non-coding RNAs (lncRNAs) facilitates to the development of effective therapeutic targets for pneumonia. LncRNA NEAT1 was vital and functional in inflammatory diseases but has not been studied in pneumonia. The aim of this study was to investigate the role of NEAT1 in pneumonia and explore its potential mechanism. Lipopolysaccharide (LPS) was applied into WI-38 cells to establish cell model of pneumonia. Cells were transfected with shRNA-NEAT1, miR-193a-3p or negative control. Real time quantitative PCR and western blot were performed to detect mRNA level and protein expression, respectively. Cell counting kit-8 (CCK-8) assay was performed to detect cell viability. Flow cytometry analysis was performed to determine cell apoptosis. Cell viability was significantly declined and cell apoptosis was increased in LPS-treated WI-38 cells. NEAT1 was upregulated under LPS treatment and NEAT1 inhibition significantly improved cell viability, decreased cell apoptosis and the production of inflammatory cytokines. The expression level of miR-193a-3p was regulated by NEAT1, and NEAT1 reversed miR-193a-3p overexpression-alleviated inflammatory injury that include inflammation and apoptosis induced by LPS. Further, NEAT1 and miR-193a-3p regulated the activity of Toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB) signaling. Therefore, NEAT1 may function as a ceRNA by sponging miR-193a-3p to regulate the activation of TLR4/NF-κB signaling to alleviate inflammation and apoptosis of WI-38 cells induced by LPS, thus influencing the development of pneumonia. Our findings implied that NEAT1 might serve as a neoteric therapy target for pneumonia.