CAV-1 KO BM from mice with established PH transfers the disease to WT Mice.CAV-1 KO or WT mice were exposed to hypoxia to induce PH. BM cells were isolated and transplanted in naive WT mice. BM from mice under normoxia used as control transplantation. Recipient mice were analyzed 5 months posttransplant. (A) Schematic representation of the BM transplant experiments. (B) Pulmonary vessel density was measured on lung tissue sections stained for endothelial cell marker CD31. CD31 area/total lung tissue area was quantified and showed that transplantation of CAV-1 KO BM from mice with established PH (hypoxia) induced endothelial remodeling in the lungs of WT recipient mice. (C) Measurement of RVSP by SPR-1000 Mikro-Tip Catheter into the right ventricle demonstrated that CAV-1 KO BM engraftment to WT mice led to elevations in RVSP. (D) Quantification of RV cardiomyocyte area to analyze RV hypertrophy. CAV-1 KO BM from mice with established PH induced hypertrophy of cardiomyocytes in the RV. (E) RV fibrosis was quantified on RV tissue sections stained with trichrome. Trichrome area/total RV area was quantified, and there was no difference across the group, suggesting that the hypertrophy of cardiomyocytes was an adaptive response. Each group contained 4 male mice. Mean ± standard error values are shown. ANOVA values show differences across groups. Symbols represent significant differences between 2 groups (P < .05): #WT normoxia vs CAV-1 KO normoxia; ∼WT hypoxia vs CAV-1 KO normoxia; §WT normoxia vs CAV-1 KO hypoxia; *WT normoxia vs WT hypoxia; ¶WT hypoxia vs CAV-1 KO hypoxia; ¤CAV-1 KO normoxia vs CAV-1 KO hypoxia.