MicroRNA‐144‐3p controls the apoptosis of pulmonary artery endothelial cells in pulmonary arterial hypertension via the BMPR2/Smad4 signaling pathway

Background This study was to determine the molecular mechanism of miR-144-3p in treatment pulmonary arterial hypertension (PAH). Methods Luciferase assays detected binding site miR-144-3p. Quantitative reverse transcription-polymerase chain reaction (PCR) measured expression downstream genes Smad4 artery endothelial cells (PAECs). Cell apoptosis analysed by fluorescence activated cell sorting (FACS) analysis. In a monocrotaline-induced rat PAH model, integrity PAECs hematoxylin eosin (H&E) staining, immunohistochemistry, and immunofluorescence. The protein bone morphogenetic receptor 2 (BMPR2)/Smad4 signaling pathway Western blotting. Results MiR-144-3p targeted directly down-regulated α-smooth muscle actin (SMA), Connective tissue growth factor (CTGF) c-myelocytomatosis (MYC) PAECs. There significant change transfected with After transfection, phosphorylation decreased only at 24 h. improved down-regulation BMPR2, Smad1/5 p-Smad1/5 group. fold p-Smad4 significantly PAH-miR Moreover, we observed α-SMA, CTGF c-MYC an up-regulation vascular (VE)-cadherin. Conclusions modulates phenotype switching via BMPR2/Smad4 pathway.