| Popis: |
MiR30a plays diverse roles in inflammatory diseases, including autoimmune hepatitis (AIH). Klf14 is associated with the inflammation in AIH. We investigated whether miR30a exerts its regulatory function via Klf14. Concanavalin A (Con A)-induced AIH mice were infected with a miR30a agomir or antagomir. MiR30a expression was quantified using qRT-PCR. TargetScan and luciferase reporter assays were used to predict the relationship between miR30a and Klf14. Liver inflammation was evaluated by measuring serum alanine transaminase (ALT) and aspartate aminotransferase (AST) levels, performing histology, and measuring mRNA expressions of inflammatory cytokines and Klf14 by qRT-PCR, protein of Klf14 by western blotting, and Tregs by FACS. MiR30a was downregulated in the hepatocytes (HCs) of AIH mice, which was negatively associated with the liver inflammation. MiR30a overexpression alleviated the inflammation, whereas downregulation of endogenous miR30a aggravated it. The mRNA and protein level of Klf14 were inversely correlated with the miR30a expression. The luciferase reporter assay validated the relationship between Klf14 and miR30a. Moreover, the frequency of Tregs was consistently correlated with the expression of miR30a. MiR30a may play an essential role in AIH, and its ability to regulate the inflammatory responses may, at least partially, be mediated by targeting Klf14 to modulate Tregs. |
