Fig. 3: Effects of B38-CAP on angioteinsin II-induced cardiac hypertrophy and fibrosis.
From: B38-CAP is a bacteria-derived ACE2-like enzyme that suppresses hypertension and cardiac dysfunction
a–c Cardiac hypertrophy in the mice chronically co-treated with Ang II (1.5 mg kg−1 per day) and B38-CAP (3 mg kg−1 per day) in the cohort of Fig. 2d–h. Macroscopic heart images (a), heart weight to body weight ratio (HW/BW) (b), and heart weight to tibia length ratio (HW/TL) (c) in mice treated vehicle + vehicle (n = 10), vehicle + B38-CAP (n = 11), Ang II + vehicle (n = 11), and Ang II + B38-CAP (n = 11). Bars indicate 2 mm. d–f Echocardiography parameters of left ventricular end-diastolic posterior wall thickness (PWD) (d), end-diastolic interventricular septal wall thickness (IVSD) (e), and %fractional shortening (%FS) (f) in the mouse hearts. Complete echocardiography data are shown in Supplementary Table 2. g, h Histology of hearts. Masson’s trichrome staining (g); bars indicate 2 mm and 100 μm in the upper panels and lower panels, respectively. Quantification of fibrosis in the hearts (h) of mice treated with vehicle + vehicle (n = 5), vehicle + B38-CAP (n = 5), Ang II + vehicle (n = 7), and Ang II + B38-CAP (n = 8). i–k qRT-PCR analysis of pro-fibrotic gene expressions in the hearts of mice treated with vehicle + vehicle (n = 5), vehicle + B38-CAP (n = 5), Ang II + vehicle (n = 7), and Ang II + B38-CAP (n = 8); mRNA levels of Collagen 8a (Col8a1) (f), Periostin (Postn) (g), and TGF-β (Tgfb2) (h) normalized with Gapdh. All values are means ± SEM. b–f, h–k Two-way ANOVA with Sidak’s multiple-comparisons test. Numbers above square brackets show significant P-values.
