MicroRNA-155 Regulates Human Angiotensin II Type 1 Receptor Expression in Fibroblasts

摘要: A large number of studies have demonstrated that the expression angiotensin II type 1 receptor (AT1R) is regulated predominantly by post-transcriptional mechanisms. Recently, it has been suggested 10% human genes may be regulated, in part, a novel mechanism involving microRNAs (miRNAs). miRNAs are small RNAs regulate gene primarily through translational repression. The aim this study was to determine whether could AT1R expression. Luciferase reporter assays miR-155 directly interact with 3′-untranslated region hAT1R mRNA. Functional transfection into primary lung fibroblasts (hPFBs) reduced endogenous compared non-transfected cells. Additionally, transfected cells showed significant reduction II-induced extracellular signal-related kinase 1/2 (ERK1/2) activation. Furthermore, when hPFBs were an antisense inhibitor, anti-miR-155, and ERK1/2 activation significantly increased. Finally, transforming growth factor-β1 treatment resulted decreased increased hAT1R. In summary, our suggest can bind (UTR) mRNAs translationally repress protein vivo. Importantly, repression mediated physiological stimuli.