Effects of silencing miR-142-3p on the pathological and physiological functions of cardiac fibroblasts

MicroRNAs (miRs), a group of small and non-coding RNAs, negatively regulate gene expression via promoting messenger RNA (mRNA) degradation or blocking mRNA translation. Many miRs have been recognized as biomarkers or possible targets for the diagnosis or therapy of some diseases. Among them, miR-142-3p was involved in the occurrences and progression of various cardiovascular diseases. Previous studies found that miR-142-3p upregulation could ameliorate myocardial ischemia/reperfusion (I/R)-induced transdifferentiation of fibroblasts to myofibroblasts and collagen deposition. miR-142-3p-mediacted autophagy was reported as a novel mechanism towards I/R-induced cardiac injure. Besides, miR-142-3p could mitigate myocardial mitochondrial dysfunction. Thus, it is worth studying whether silencing miR-142-3p may affect the pathological and physiological functions of cardiac fibroblasts. We treated cardiac fibroblasts with NC or miR-142-3p antagomiR (n=3).Briefly, 50nM miR-142-3p antagomir or NC was transfected into CFs using Lipofectamine RNAiMAX (Invitrogen, Carlsbad, CA, USA) following the manufacturers’ instructions. Then, all samples were used for transcriptome RNA sequencing. Comparative gene expression profiling analysis of RNA-seq data was then performed.