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Fig. 5 | Respiratory Research

Fig. 5

From: CRISPR-mediated Bmpr2 point mutation exacerbates late pulmonary vasculopathy and reduces survival in rats with experimental pulmonary hypertension

Fig. 5

Phenotypic 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 isoform

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