miR-351-5p aggravates lipopolysaccharide-induced acute lung injury via inhibiting AMPK

Inflammation and oxidative stress have indispensable roles in the development of acute lung injury (ALI). MicroRNA (miRNA/miR)-351-5p was initially identified as a myogenesis-associated miRNA; however, its role in lipopolysaccharide (LPS)-induced ALI remains unclear. The aim of the present study was to investigate the role and potential mechanisms of miR-351-5p in ALI. ALI was induced through a single intratracheal injection of LPS for 12 h, and miR-351-5p agomir, antagomir or their corresponding negative controls were injected into the tail vein before LPS stimulation. Compound C, 2 ',5 '-dideoxyadenosine and H89 were used to inhibit AMP-activated protein kinase (AMPK), adenylate cyclase and protein kinase A (PKA), respectively. miR-351-5p levels in the lungs were significantly increased in response to LPS injection. miR-351-5p antagomir alleviated, while miR-351-5p agomir aggravated LPS-induced oxidative stress and inflammation in the lungs. The present results also demonstrated that miR-351-5p antagomir attenuated LPS-induced ALI via activating AMPK, and that the cAMP/PKA axis was required for the activation of AMPK by the miR-351-5p antagomir. In conclusion, the present study indicated that miR-351-5p aggravated LPS-induced ALI via inhibiting AMPK, suggesting that targeting miR-351-5p may help to develop efficient therapeutic approaches for treating ALI.

Automated summary

The study shows that miR-351-5p exacerbates LPS-induced ALI by inhibiting AMPK, and targeting this miRNA may be a promising therapeutic approach for treating ALI. MiR-351-5p antagomir attenuates LPS-induced ALI by activating AMPK and utilizing the cAMP/PKA axis.