MiR-647 Targeting PRKCA to Regulate the Activation of Human Atrial Fibroblasts Through TGFβ1/Smad Pathway

Background Atrial remodeling is the main pathogenesis of atrial fibrillation (AF). Interstitial fibrosis is an important part of atrial remodeling, mainly involving the activation of atrial fibroblasts. Nowadays, studies have focused on miRNAs in regulating fibroblasts in AF related atrial fibrosis, however, the molecular mechanism of this pathological process is not fully understood. Methods Cell experiments were carried out to investigate the mechanism of miR-647 targeting PRKCA gene in regulating atrial fibrosis of AF. CCK-8, transwell, immunofluorescence assays were applied to observe the proliferation, migration and the phenotypic transformation of the human atrial fibroblasts. qRT-PCR and WB were used to detect the collagen production, expression levels of α-SMA and TGFβ1/Smad pathway. Results The results of CCK-8, transwell and immunofluorescence assays showed that miR-647 inhibited the proliferation, migration and the fluorescence intensity of α-SMA of the human atrial fibroblasts. QRT-PCR and WB showed that miR-647 could significantly attenuate the expression levels of fibrosis related Collagen I and III, α-SMA and TGFβ1/Smad pathway by targeting PRKCA. Conclusion MiR-647 targeting PRKCA gene regulates the activation of human atrial fibroblasts through the TGFβ1/Smad pathway.