Fig. 2
Cardiac-specific deletion of Tet2 and Tet3 resulted in developmental defects in the ventricular chamber. a Genotyping analysis from Tet2−/−Tet3flox/flox and Tet2+/−Tet3flox/flox;Nkx2.5-Cre interbreedings. *p < 0.05, **p < 0.01 (chi-squared test were used). b (Top) Representative H&E staining images of embryonic heart tissues (×4) collected at E12.5, 13.5, 14.5, and 15.5 stages from control and Tet2/3-DKO mice. (Bottom) Quantifications were performed by using the Image J software. Data were shown as mean ± S.D; n = 36 sections from 3 independent experiments. **p < 0.01 compared to control (two-tailed Student’s t-test were used). Scale bar: 300 µm. c Real-time qPCR to quantify the expression of Nppa and Hey2 in control and Tet2/3-DKO embryonic heart tissues collected at E12.5. Data were shown as mean ± S.D; n = 3 independent experiments. **p < 0.01 (two-tailed Student’s t-test were used). d (Left) Representative fluorescent imaging of embryonic heart tissues collected from E12.5 of control (top) or Tet2/3-DKO mice (bottom). DAPI (blue) was used for nuclear staining; Ki67 (red) was used as a proliferation marker; and cTnT (yellow) was used as the staining marker for cardiomyocytes. Cells demarcated within the white dashed lines are blood cells. (Right) Quantifications of the percentage of cardiomyocytes with positive Ki67 staining. Data were shown as mean ± S.D; n = 4 independent experiments (a total of 525 and 568 cardiomyocytes were quantified from control and Tet2/3-DKO embryos, respectively). *p < 0.05 compared to control (two-tailed Student’s t-test were used). Scale bar: 50 µm
