Fig. 1

A Pulmonary hypertension phenotype assessment in SD rats. Adult male Sprague Dawley rats (320–370 g) were randomly assigned into air or hypoxic chamber with 10% oxygen for 1 or 28 days. After pulmonary hemodynamic assessment for right ventricular systolic pressure (RVSP), mean pulmonary artery pressure (mPAP), pulmonary vascular resistance (PVR) and right ventricle hypertrophy [right ventricular weight/left ventricular plus septal weight, RV/(LV + S)], n = 6 for each, *P < 0.05. Pulmonary artery smooth muscle cells (PASMCs) were mechanically removed carefully from intra-lobe pulmonary arteries and subjected to ATAC-seq and RNA-seq. B Genomic distribution of differential accessibility regions (DARs). C Comparison of genes annotated with DARs including opened or closed chromatin accessibility (left and middle) and homologues with human (right). D Comparison of differentially expressed genes (DEGs) including up-regulated and down-regulated genes (left and middle) and homologues with human (right). E Comparison of DARs and DEGs. F Pearson correlation analysis of RNA-seq and ATAC-seq in PASMCs of rats after exposure to hypoxia for 1- (upper) or 28-days (lower), fold change > 2, P > 0.05 as compared to normoxia. G Comparison of DEGs and DARs in promoter region. All in PASMCs of rats after exposure to hypoxia for 1- or 28-days, fold change > 2, P < 0.05 as compared to normoxia (B, C, D, E and G)