fig3

Effects of tamoxifen inducible MerCreMer on gene expression in cardiac myocytes in mice

Figure 3. Histological evaluation of the myocardium in the Myh6-Mcm mice injected with tamoxifen (TAM) at 4 weeks of age. (A) Picrosirius red-stained thin myocardial sections in the wild type and Myh6-Mcm (injected with TAM) mice at 4 weeks of age, showing no evidence of myocardial fibrosis. (B) Quantitative data of myocardial fibrosis presented as collagen volume fraction (CVF) in the experimental groups. (C) Assessment of apoptosis by the transferase deoxyuridine triphosphate (dUTP) nick end labeling (TUNEL) assay in the myocardial sections from the wild type and Myh6-Mcm (injected with TAM) mice, showing rare cells stained for TUNEL in green. Nuclei are stained with 4′,6-diamidino-2-phenylindole (DAPI) and shown in blue color. (D) Quantitative data showing the percentage of nuclei stained for TUNEL in each experimental group. (E) Immunofluorescence panel showing thin myocardial sections stained for phospho-the histone protein family member X (H2AFX) in the wild type and Myh6-Mcm (injected with TAM) mice, showing scattered positive cells. (F) Quantitative data showing the percent of phospho-H2AFX stained nuclei in the experimental groups. (G) Immunoblot analysis of cardiac myocyte protein extracts of wild type and Myh6-Mcm (injected with TAM) mice detecting phospho-H2AFX and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) [Supplementary Figure 1]. (H) Quantitative analysis of immunoblots detecting the phospho-H2AFX protein levels normalized to the GAPDH protein levels.

The Journal of Cardiovascular Aging

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