MiR-181b Targets Semaphorin 3a to Mediate TGF-β-induced Endothelial to Mesenchymal Transition: Implication in Atrial Fibrillation

Background:This study investigated if and how atrial endothelial cells may transform to mesenchymal cells and contribute to atrial fibrosis via endothelial-to-mesenchymal transition (EndMT). Results:We show a novel mechanistic link between TGF-β1/SMAD signaling and decreased Sema3a expression through the induction of miR-181b; this pathway plays an important role in EndMT associated with the pathogenesis of AF. Both miR-181b and Sema3a are potential therapeutic targets in AF. The AAECs were isolated from 3 patients and were treated TGFbeta(5ng/mL) for 24hr to mimic the pathogenesis and performed miRNA arrays