Omentin Modulates Chronic Cardiac Remodeling After Myocardial Infarction

Figures

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  Figure 1.. Kaplan-Meier survival analysis of wild-type mice (WT; n=40) and transgenic mice expressing the human omentin gene in fat tissue (OMT-Tg; n=42) after myocardial infarction.

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  Figure 2.. Transgenic mice expressing the human omentin gene in fat tissue (OMT-Tg) mice show improvement in cardiac dysfunction after myocardial infarction (MI). (A, Left) Representative cross-sections of heart tissue stained with Masson’s trichrome 4 weeks after MI in wild-type (WT) and OMT-Tg mice. Scale bars, 2.5 mm. (A, Right) Quantitative analysis of the infarct size as a percentage of left ventricular (LV) circumference in WT (n=8) and OMT-Tg mice (n=9). Data are the mean±SEM. (B,C) Heart weight (HW) to body weight (BW) ratios (B) and lung weight to BW ratios (C) in WT and OMT-Tg mice 4 weeks after MI or sham surgery. Data are the mean±SEM (n=8–9 in each group). (D) Representative M-mode echocardiograms 4 weeks after MI or sham operation in WT and OMT-Tg mice. (E) Left ventricular diastolic diameter (LVDd) and (F) percentage fractional shortening (FS) in WT and OMT-Tg mice 4 weeks after MI or sham surgery. Data are the mean±SEM (n=8–9 in each group).

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  Figure 3.. Capillary density, myocardial apoptosis, interstitial fibrosis and cardiomyocyte size in post-myocardial infarction (MI) hearts from wild-type (WT) mice and transgenic mice expressing the human omentin gene in fat tissue (OMT-Tg). (A, Left) Representative photographs of anti-CD31-stained heart samples from WT and OMT-Tg mice at 4 weeks after MI or sham operation. Scale bars, 50 μm. (A, Right) Quantitative analysis of CD31-positive capillary density in heart tissue of WT and OMT-Tg mice. Data are the mean±SEM (n=8 in each group). (B, Left) Representative images of terminal deoxyribonucleotidyl transferase-mediated dUTP–digoxigenin nick end-labeling (TUNEL)-stained heart tissue sections 4 weeks after MI or sham operation. TUNEL staining (green) identifies apoptotic nuclei; and 4′,6-diamidino-2-phenylindole (DAPI; blue) identifies total nuclei. (B, Right) Quantitative analysis of TUNEL-positive cells in hearts from WT and OMT-Tg mice. The frequency of TUNEL-positive cells was calculated as the percentage of DAPI-positive nuclei among the total number of nuclei. Data are the mean±SEM (n=8 per group). (C, Left) Masson’s trichrome staining of heart sections from WT and OMT-Tg mice 4…

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  Figure 4.. Inflammatory response, oxidative stress, and AMP-activated protein kinase activation in post-MI hearts from wild-type (WT) mice and transgenic mice expressing the human omentin gene in fat tissue (OMT-Tg). (A,B) Myocardial levels of tumor necrosis factor (TNF)-α (A) and p47phox (B) in WT and OMT-Tg mice 4 weeks after MI or sham operation. Data are the mean±SEM (n=6 in each group). mRNA levels were quantified by real-time polymerase chain reaction (PCR) analysis and presented relative to levels of β-actin. (C) Phosphorylation (p) of AMPK and Akt in heart tissues from WT and OMT-Tg mice 4 weeks after MI, as determined by western blot analysis. Data are the mean±SEM (n=4 in each group).

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  Figure 5.. Supplementation of wild-type (WT) mice with omentin after myocardial infarction (MI) improves cardiac remodeling. Four days following MI, adenoviral vectors that expressed omentin (Adeno-OMT) or β-galactosidase (Adeno-βgal) were administered to WT mice (used as the control). (A) Quantification of infarct size as a percentage of left ventricular (LV) circumference in Adeno-βgal-treated or Adeno-OMT-treated mice 4 weeks after MI. (B) Heart weight (HW) to body weight (BW) ratio and (C) lung weight to BW ratio in Adeno-βgal-treated or Adeno-OMT-treated mice 4 weeks after MI. (D) Left ventricular diastolic diameter (LVDd) and (E) percentage fractional shortening (FS) in Adeno-βgal-treated or Adeno-OMT-treated mice 4 weeks after MI. Data are the mean±SEM (n=3 for Adeno-OMT mice; n=6 for Adeno-βgal mice).