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. 2021 Jan 1;11(3):1249–1268. doi: 10.7150/thno.48787

Figure 5.

Figure 5

Knockdown of Wnt5a and Wnt11 inhibits cardiac fibrosis in mice under pressure overload. (A), Overall strategy to explore cardiac remodeling after knockdown of Wnt5a and Wnt11 in mice under pressure overload. (B), Fraction shortening (FS) in mice at 4 weeks after TAC. Mice were injected with sh-Wnt5a/Wnt11-AAV9 (sh-Wnt5a/Wnt11) or sh-scramble-AAV9 (shNC) by tail vein two weeks before TAC or sham operation. *p < 0.05; n = 6-10/each group. (C), Masson staining of heart tissue from mice in (B) and fibrosis area was quantitatively analyzed. Bar = 100 µm. *p < 0.05; ***p < 0.001. n = 4-9/each group. (D), Western blot analysis of Wnt5a, Wnt11, Col1, Col3, MMP9, TGF-β1, α-SMA, and p-smad2/3 expression in heart tissue from TAC or sham mice pre-injected with sh-Wnt5a/Wnt11-AAV9 (sh-Wnt5a/Wnt11) or sh-scramble-AAV9 (sh-NC) by tail vein. **p < 0.01; ***p < 0.001. n = 4-6 mice/each group. (E), Western blot analysis of Col1, MMP2, MMP9, TGF-β1 and α-SMA expression in CFs stimulated with the culture medium from control (Ad-CON) or LRP6 overexpressing CMs (Ad-LRP6), Wnt5a, Wnt11, Wnt5a+Wnt11 at 10 ng/mL, or PBS were supplemented with the culture medium from Ad-LRP6-CMs under MS and treated with CFs. *p < 0.05; **p < 0.01; ***p < 0.001. n = 3/each group.