STAT3-activated lncRNA XIST accelerates the inflammatory response and apoptosis of LPS-induced acute lung injury.

Abstract

Acute lung injury (ALI) is a severe lung respiratory failure characterized by high morbidity and mortality. Novel findings demonstrated the critical roles of long non‐coding RNA (lncRNA) in ALI. Here, we tried to investigate the roles and potential mechanism of lncRNA X‐inactive specific transcript (XIST) in ALI. Results illustrated that lncRNA XIST was up‐regulated in the lipopolysaccharide (LPS)‐induced ALI mice models and pulmonary endothelial cells. Biofunctional assays unveiled that knockdown of XIST repressed the inflammatory response and apoptosis in LPS‐induced endothelial cells. Mechanistically, XIST acted as the miR‐146a‐5p sponge to positively regulate STAT3. Moreover, STAT3 combined the promoter region of XIST to accelerate the transcription, constituting the positive feedback loop of XIST/miR‐146a‐5p/STAT3 in ALI. Collectively, these findings suggested that XIST knockdown attenuates the LPS‐induced ALI, providing a potential therapeutic target.