Fig. 7

TRB3 knockdown reversed and prevented the progression of hypoxia -induced PH. A The right ventricular systolic pressure(RVSP) was measured by a 1.2-Fr pressure catheter (GuGeShengWu, Wuhan, China) inserted via the right jugular vein and positioned in the right ventricle. B The values of RVSP were obtained using the ADInstruments Powerlab data acquisition system. C Right ventricular hypertrophy was evaluated by the ratio of the RV/(LV + S). The right ventricle (RV) was peeled off from the left ventricle (LV) and the septum (S), and the dry weight of the two components was measured. D Systemic blood pressure was measured by a 1.2-Fr pressure catheter inserted via the left carotid artery. E Lung tissue sections were stained for hematoxylin–eosin (HE) (magnification, × 200) and α-SMA (magnification, × 400). F Pulmonary vascular remodeling was evaluated by the percentage of medial wall thickness of distal pulmonary vessels, which was expressed using the following equation: [(external diameter − internal diameter)/external diameter]. G The whole pulmonary artery of each rat from different groups was extracted, and TRB3 protein expression in each group was measured by western blot analysis. H and I PCNA protein expression in pulmonary arteries was examined by immunohistochemical staining and western blot analysis. J MMP9 protein expression in pulmonary arteries was examined by western blot analysis. K The phosphorylated forms of ERK, JNK, and p38 MAPK in pulmonary arteries in each group were evaluated by western blot analysis. Data represent the mean ± SEM (n = 4). *P < 0.05 and **P < 0.01