Fig. 3

Cardiomyocyte-specific overexpression of NHE1 alleviates cardiac damage caused by MI with acute hyperglycemia. A Schematic showing the strategy for cardiomyocyte-specific NHE1 overexpression (AAV9-Control, Con; AAV9-NHE1, NHE1) B Western blot analysis and quantification of NHE1 protein levels in extracts from heart samples of Con and NHE1 mice without MI with acute hyperglycemia (n = 3 for each group). C Schematic showing the experimental design for Con and NHE1 mice during MI with acute hyperglycemia. D and E The ratios of heart weight to body weight (HW/BW) and heart weight to tibia length (HW/TL) in Con and NHE1 mice (n = 10 per group). F Representative M-mode echocardiographic images of heart ultrasound recording at baseline and day 7 post MI with acute hyperglycemia (scale bar, 100 ms and 1 mm) for Con and NHE1 mice. G Comparison of EF at day 7 post MI with acute hyperglycemia in Con and NHE1 mice (n = 10 per group). H Representative Masson's trichrome staining (up) and Picrosirius red staining (down) in Con and NHE1 mice at day 7 post MI with acute hyperglycemia, scale bar, 1 mm. I and J Quantification of cardiac fibrosis in total tissue area and LV wall thickness in Con and NHE1 mice, n = 8 (Con) and n = 7 (NHE1). K and L Images and quantitative results of cardiac IgG immunostaining (red signals) in mouse hearts, whole heart sections were stained with WGA, n = 3 (Con) and n = 4 (NHE1). Scale bar, 500 μm. M Analysis of serum BNP levels between Con and NHE1 mice at 7 day post-MI with acute hyperglycemia, n = 8 (Con) and n = 7 (NHE1). Statistical significance in B, C, D, E, G, I, J, L and M were determined using two-tailed unpaired student’s t test. All quantitative data are expressed as mean ± SD