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

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.

Automated summary

Research has shown that lncRNA XIST plays a crucial role in ALI by positively regulating STAT3 to affect inflammatory response and cell apoptosis, providing a potential therapeutic target for ALI treatment.