LncRNA NEAT1 exacerbates sepsis-induced acute lung injury via targeting miR-26a-5p/ROCK1 axis

Abstract

Background: Acute lung injury (ALI) is a severe disease of respiratory system, which one of the most common causes is sepsis induction. Cell apoptosis and inflammation contribute to the progression of ALI and lncRNAs play crucial roles in ALI. Hence, this study is to unearth the specific mechanism of NEAT1.Methods: BEAS-2B cells was exposed to lipopolysaccharide (LPS) to construct cell model of sepsis-induced ALI. The gene and protein expression were evaluated using qRT-PCR and western blot. Cell viability was determined by CCK-8. Cell apoptosis was detected utilizing flow cytometry. The secretion of inflammatory factors was assessed using ELISA. The interconnections among NEAT1, miR-26a-5p and ROCK1 were validated using starbase, luciferase assay and RIP.Results: LPS treatment elevated NEAT1 and ROCK1 levels while reduced miR-26a-5p level in BEAS-2B cells. Besides, LPS treatment augmented cell apoptosis and enhanced inflammatory cytokine secretion, whereas NEAT1 silencing could reversed LPS-mediated these influences in BEAS-2B cells. Mechanistically, NEAT1 positively mediated ROCK1 expression through targeting miR-26a-5p. Moreover, miR-26a-5p inhibitor offset NEAT1 depletion-mediated suppressive influences on cell apoptosis and inflammation. ROCK1 upregulation attenuated the inhibitory impacts generated by miR-26a-5p overexpression on cell apoptosis and inflammation. Conclusion: Our results revealed NEAT1 could reinforce LPS-induced cell apoptosis and inflammatory response through repressing miR-26a-5p/ROCK1 axis, thereby aggravating ALI caused by sepsis. Our data suggested NEAT1, miR-26a-5p and ROCK1 might be biomarkers and targets genes for alleviating sepsis-induced ALI.