Fig. 9
Analysis of fibrosis in mice hearts after treatment with angiotensin II and hiPS-EVs. Mice received angiotensin II for 14 (group Ang14) or 28 days (the rest of the animals) in osmotic pumps implanted subcutaneously. Next, they were treated with hiPS-EVs derived from normoxia (EV-N) or hypoxia 5% O2 (EV-H5). Control animals received PBS only (group PBS). A Microscopic images of collagen staining in mouse hearts using the Sirius red dye. Cross-sections (upper panel) and zoomed areas (lower panel) are presented. B Analysis of transcript levels of key genes involved in fibrosis (Acta2, Col1a1, Col3a1, Ctgf), performed by real-time qPCR (n = 5–6). C Analysis of pro-fibrotic proteins (α-Sma, Col1a1, and Col3a1) by Western blot. D Densitometric analysis of the protein levels normalized to the level of control protein (Vinculin) (n = 5–6). All data are presented as the mean ± SD. Statistical significance was tested using one-way ANOVA with the Tukey post hoc test (B, D — Col3a1) or Kruskal–Wallis and Dunn’s post hoc test (D — α-Sma, Col1a1). *p < 0.05; **p < 0.01; ***p < 0.001