Fig. 5From: CRISPR-mediated Bmpr2 point mutation exacerbates late pulmonary vasculopathy and reduces survival in rats with experimental pulmonary hypertensionPhenotypic changes of medial smooth muscle cells in the lungs of rats with Bmpr2 mutation. Immunohistochemical staining of the pulmonary arteries (PAs) in male rats at 3 weeks after monocrotaline injection using smooth muscle cell differentiation state specific markers, α-smooth muscle actin (SMA), smooth muscle myosin heavy chain SM-2 (SM-2, as a mature phenotypic marker) and nonmuscle myosin heavy chain SMemb (SMemb, as an immature phenotypic marker). A–I Representative immunohistochemistry images and semi-quantitative analysis indicated by grade for α-SMA, SM-2 and SMemb positive cells in proximal PAs in wild-type (WT) and Bmpr2 mutant (+/44insG) rats, respectively (n = 6). Scale bar: 50 μm. J–R Representative immunohistochemistry images and semi-quantitative analysis indicated by grade for α-SMA, SM-2 and SMemb positive cells in distal PAs in WT and +/44insG respectively (n = 6). Scale bar: 50 μm. S and T Representative Western blots and the quantification of relative α-SMA (S, n = 4 for each group) and SM-2 (T, n = 3 for each group) protein expression in the lung tissue of WT and +/44insG rats respectively. The numbers in parentheses represent the numbers of rats examined. The data are presented as means ± SEM; unpaired t-test was used for analysis; **p < 0.01, ***p < 0.001. PAs = pulmonary arteries; WT = wild-type; +/44insG = rats with bone morphogenetic protein receptor type 2 mutation; α-SMA = α-smooth muscle actin; SM-2 = smooth muscle myosin heavy chain SM-2; SMemb = nonmuscle myosin heavy chain embryonic isoformBack to article page