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. 2022 Jul 1;132(13):e142548. doi: 10.1172/JCI142548

Figure 7. Antagomir-181b inhibits the development of atrial subendocardial fibrosis in TGF-β–transgenic mice.

Figure 7

(A) Design and optimization of the appropriate treatment strategy. (B) Histological morphology analysis of trichrome-stained atrial tissue demonstrating collagen (blue) deposition. Scale bar: 25 μm. (C) Quantitative analysis of endocardial fibrotic tissue thickness, (D) miR-181b expression in atrial tissue lysates, (E) AF duration, and (F) AF inducibility. (C–F) Data are presented as the mean ± SEM (n = 5–7 per group). **P < 0.01 and ***P < 0.001 versus WT mice; #P < 0.05 and ##P < 0.01, versus TGF-β–transgenic mice; 1-way ANOVA with Bonferroni’s post hoc test. (G) Immunohistochemical analysis of CD31 with Sema3A, Twist, SMA and vimentin in the endocardium (n = 5). Scale bars: 50 μm. (H) Western blot analysis of proteins in atrial tissue from WT, TGF-β–transgenic mice (TGF transgene), and TGF-β–transgenic mice with antagomir-181b treatment showing increased SMA, Twist, vimentin, Snail, Slug, SM22α, and collagen I levels but decreased Sema3A and VE-cadherin levels in TGF-β–transgenic mice compared with WT mice. TGF-β–transgenic mice with antagomir-181b treatment showed a reversal of Sema3A and VE-cadherin protein levels and reduced expression of EndMT markers.