Abstract
Pneumonia is a common respiratory disease worldwide. Long noncoding RNAs have been implicated in the pathogenesis of pneumonia. However, the effect and mechanism of long intergenic nonprotein-coding RNA (LINC00707) on pneumonia pathogenesis were still unclear. Lipopolysaccharide (LPS) reduced cell viability and promoted apoptosis and inflammation in MRC-5 cells. LINC00707 was increased, and miR-223-5p was decreased in LPS-treated MRC-5 cells. LINC00707 knockdown relieved LPS-triggered injury in MRC-5 cells. LINC00707 directly interacted with miR-223-5p through acting as a miR-223-5p sponge. Moreover, miR-223-5p mediated the regulation of LINC00707 silencing on LPS-stimulated cytotoxicity in MRC-5 cells. p38 mitogen-activated protein kinases and nuclear factor-κB signaling pathways were modulated by the LINC00707/miR-223-5p axis in LPS-induced MRC-5 cells. Our present study indicated that LINC00707 depletion alleviated LPS-induced injury in MRC-5 cells at least partly by acting as a sponge of miR-223-5p, highlighting a new potential therapeutic avenue for pneumonia treatment.