MicroRNA-598 inhibition ameliorates LPS-induced acute lung injury in mice through upregulating Ebf1 expression

In this study, we found that the expression of miR-598 was significantly upregulated in the lung tissues of mice with lipopolysaccharide (LPS)-induced acute lung injury. Both loss-of-function and gain-of-function studies were performed to evaluate the function of miR-598 in acute lung injury. The results showed that inhibition of miR-598 attenuated inflammatory response, oxidative stress, and lung injury in mice treated with LPS, while overexpression of miR-598 exacerbated the LPS-induced acute lung injury. Mechanistically, transcription factor Early B-cell Factor-1 (Ebf1) was predicted and validated as a downstream target of miR-598. Overexpression of Ebf1 attenuated LPS-induced production of inflammatory cytokine TNF- α and IL-6, ameliorated LPS-induced oxidative stress, promoted proliferation, and inhibited apoptosis in murine lung epithelial-15 (MLE-15) cells. Moreover, we demonstrated that Ebf1 knockdown abolished the protective effect of miR-598 inhibition in LPS-treated MLE-15 cells. In summary, miR-598 inh ibition ameliorates LPS-induced acute lung injury in mice through upregulating Ebf1 expression, which might provide potential therapeutic treatment for acute lung injury.
Source: Histochemistry and Cell Biology - Category: Biomedical Science Source Type: research