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. Author manuscript; available in PMC: 2016 Oct 1.
Published in final edited form as: Circ Cardiovasc Genet. 2015 Jul 31;8(5):665–676. doi: 10.1161/CIRCGENETICS.115.001138

Figure 5.

Figure 5

Maternal diabetes impairs the non-canonical Wnt pathway and this impairment is abolished by SOD1 overexpression. A, mRNA levels of Wnt5a in E12.5 hearts. B, Wnt5a protein levels in E12.5 hearts. C, images of Wnt5a immunostaining. Rabbit normal IgG served as controls. Red signal was Wnt5a and cell nuclei were stained by DAPI (Blue). Three hearts from embryos of three dams (n = 3) per group, and three serial sections per heart were analyzed, and similar results were obtained. Bars = 150 µm. D, levels of p-NFAT4. E, levels of nuclear NFAT2. F, levels of p-CaMKII. In B, D, E, and F, quantification of immunoblotting was shown in the dot graph. In A, B, D, E, F, experiments were repeated three times using three E12.5 hearts from embryos of three dams (n = 3) per group. * in A, B, D, E, F indicate significant difference compared to other groups. ND: nondiabetic; DM: diabetic mellitus; WT: wild-type hearts; SOD1: SOD1 overexpressing hearts.