MiR-181b targets semaphorin 3a to mediate TGF-ß-induced endothelial-to-mesenchymal transition related to 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-ß1/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. Overall design: A total of 8 mice were divided into two groups for study: wild-type mice(N=4) and TGFbeta transgene mice(N=4). Specimens of atrium from the mice were used for NGS study.