Fig 1: Effects of ARNI and SGLT2i treatment on heart-driven hormones in chronic doxorubicin-injected mice. (A) Plasma concentration of NT-proANP and (B) BNP 9 weeks after doxorubicin treatment initiation (n = 5–6/group). (C) mRNA expression of BNP and (D) ANP (n = 4–5/group). (E) Representative PAS staining of kidney cross-sections. (F) Quantitative mean glomerular volume (n = 6–7/group). (G) Plasma concentrations of BUN, (H) creatinine, and (I) NGAL 9 weeks after doxorubicin injection (n = 4–6/group). ns, no significance, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
Fig 2: Enhanced cardiomyocyte cell cycle activity observed in the simultaneous treatment of natriuretic peptide and DN-FOXO was primarily mediated through Npr3. a qRT-PCR analysis showing expression of Npr1, Npr2, and Npr3 in cultured neonatal mouse cardiomyocytes at 48 h after infection with lentivirus expressing either Npr1 shRNA, Npr2 shRNA, or Npr3 shRNA. b and c Npr3 shRNA treatment abrogating the effects of ANP/BNP and DN-FOXO effects on cardiomyocyte cell cycle activity. Quantification of cardiomyocyte cell cycle activity as the percentage of Ki67+cTnT+ (b) and EdU+cTnT+ cells (c) of total cTnT+ cells analyzed. n=4–5 per group. P value was calculated using one-way ANOVA. **P < 0.01; ***P < 0.001; ****P < 0.0001; n.s.= Not significant
Fig 3: Effect of 8 weeks CR on LV systolic function and expression or release of BNP. (A): LV fractional shortening (FS%) at the beginning of the diet (left panel) and changes in FS during the feeding period (right panel) in WT and KO sham or infarct mice, following 8 weeks of control or CR diets. (B): LV mRNA expression (left panel) and serum levels of brain natriuretic peptide (right panel) in WT and KO sham or infarct mice, following 8 weeks of control or CR diets. All data are mean ± SEM. n = 6–8 animals per group, *: p < 0.05; **: p < 0.01; ***: p < 0.001.
Fig 4: Cardiomyocyte cell cycle activity with natriuretic peptide and DN-FOXO treatment in vitro. a Isolated neonatal mouse cardiomyocytes (P1) were cultured with a medium containing Ad-Cre, ANP, BNP, or Ad-DN-FOXO for 48 h. Cardiomyocyte cell cycle activity was visualized by co-immunostaining for Ki67 (red) and cTnT (green) on cultured cardiomyocytes. Arrows point to Ki67+cTnT+ cells. b Quantification of Ki67+cTnT+ cells as a percentage of total cTnT+ cells analyzed per field (~ 1000 cTnT+ cells per sample). c Cardiomyocytes in the DNA synthesis-phase were detected by using Click-iT EdU Alexa Fluor (red) and co-immunostaining with the antibody against cTnT (green) on tissue sections. Arrows point to EdU+cTnT+ cells. d Quantification of EdU+cTnT+ cells as a percentage of total cTnT+ cells analyzed per field (~ 1000 cTnT+ cells per sample). Scale bars: 50 µm. Data are mean ± s.e.m. P value was calculated using one-way ANOVA. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001; n.s.= Not significant
Fig 5: Effect of 8 weeks CR and 2 weeks of AMPK inhibition on LV systolic function, LV weight and expression or release of BNP. (A): LV fractional shortening (FS%) at the beginning of the diet (left panel), end of the diet (middle panel), and changes in FS during the feeding period (right panel) in sham or infarct rats, following 8 weeks of control or CR diets. (B): LV weight normalized to tibia length at the end of the study (left panel), LV mRNA expression (middle panel), and serum levels of brain natriuretic peptide (right panel) in sham or infarct rats following 8 weeks of control or CR diets. All data are mean ± SEM. n = 6–7 animals per group, *: p < 0.05; **: p < 0.01; ***: p < 0.001.
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