LAUSR

Sepsis‐induced acute lung injury is associated with dysregulated inflammatory reactions. MiR‐19b‐3p level was reported to be downregulated in patients with sepsis. To evaluate the role of miR‐19b‐3p in sepsis, cecum ligation and puncture‐induced mouse sepsis model and lpopolysaccharide (LPS)‐treated pulmonary microvascular endothelial cells (PMVECs) were used. For in vivo study, lung tissue was harvested for hematoxylin and eosin (H&E) staining, tumor necrosis factor‐α, interleukin‐6 (IL‐6), IL‐1β, and p‐p65, p‐IκB measuring. Cell apoptosis was assessed by TUNEL assay. For in vitro study, cell proliferation and apoptosis were detected by CCK‐8 and flow cytometry, respectively. Methylation of miR‐19b‐3p promoter was measured by methylation‐specific PCR (MSP) assay. The target of miR‐19b‐3p was determined by dual‐luciferase reporter gene assay. The level of miR‐19b‐3p was determined to be downregulated in vitro and in vivo. In addition, miR‐19b‐3p protected mice from inflammation injury through inhibiting NF‐κB signaling pathway. Overexpression of miR‐19b‐3p increased cell viability, decreased apoptosis, and proinflammatory cytokines secretion in LPS‐treated PMVECs. Besides these, Krüppel‐like factor 7 (KLF7) was confirmed as the target of miR‐19b‐3p. And methylation of miR‐19b‐3p was the reason of decreased miR‐19b‐3p level. In conclusion, miR‐19b‐3p protected cells from sepsis‐induced inflammation injury via inhibiting NF‐κB signaling pathway, and KLF7 was a potential target.