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. 2021 Jan 1;11(4):1609–1625. doi: 10.7150/thno.48153

Figure 2.

Figure 2

Lack of inhibitory effects of simvastatin on TAC-induced cardiac fibrosis and hypertrophy after in vivo endothelial specific Klf2 inhibition. A-B, Masson's Trichrome staining shows a significant reduction of cardiac fibrosis in TAC pressure overload mice following administration of simvastatin compared with the vehicle control (A), while RGD-nanoparticle in vivo inhibition of EC-Klf2 expression attenuates the simvastatin-mediated reduction of TAC-induced increased cardiac fibrotic area compared with the nanoparticles packaging control scramble (Sc)-siRNA (B), with representative image (left) and quantification (right) (n=10). C-F, Simvastatin reduces the TAC-induced elevation of heart to body weight ratio (C) and LV mass by echocardiogram (D) as compared with the vehicle control, while RGD-nanoparticle packaging Klf2-siRNA attenuated the TAC-induced elevated heart to body weight ratio (E), LV mass (F) compared with the nanoparticles packaging control scramble-siRNA (n=10). G-H, Wheat germ agglutinin (WGA) staining shows a significant decreased size of cardiomyocytes in TAC pressure overload mice following simvastatin administration compared with the vehicle control (G), while RGD-nanoparticle Klf2-siRNA attenuates the simvastatin-mediated reduction of TAC-induced increased cardiomyocyte size (H) with representative image (left) and quantification (right) (n=10). Data are means ± S.E.M. *P<0.05, ** P<0.01 and n.s. not significant. 2-way ANOVA with Turkey test. Scale Bars: A, B, 100 µm; G, H, 50 µm.