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High-fat diet induces cardiac remodelling and dysfunction: assessment of the role played by SIRT3 loss.

Zeng H, Vaka VR, He X, Booz GW, Chen JX - J. Cell. Mol. Med. (2015)

Bottom Line: HFD resulted in a significant reduction in SIRT3 expression in the heart.SIRT3 KO mice fed HFD showed greater ROS production and a further reduction in cardiac function compared to SIRT3 KO mice on ND.However, HFD did not further reduce capillary density in SIRT3 KO hearts, implicating SIRT3 loss in HFD-induced capillary rarefaction.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology and Toxicology, The University of Mississippi Medical Center, School of Medicine, Jackson, MS, USA.

No MeSH data available.


Related in: MedlinePlus

HFD and SIRT3 loss reduce capillary density in the heart. Hearts were extracted from WT and KO mice fed ND or HFD for 16 weeks. Ventricular sections were prepared and stained with green fluorescent isolectin B4 (IB4) as an endothelial cell marker. (A) Representative images of mouse hearts from WT-ND, WT-HFD, KO-ND and KO-HFD (a, b, c and d respectively) are shown. (B) IB4 staining was quantified by Image J and normalized to DAPI staining of nuclei (relative intensity). Values are mean ± SEM, n = 3 mice per group. PI, PD and PS ≤ 0.01; *P ≤ 0.05; **P ≤ 0.01. (C) Cell proliferation assay. The proliferation of microvascular endothelial cells from WT and SIRT3 KO lungs was assessed using an MTT assay. Values are mean ± SEM, n = 5 independent observations; **P ≤ 0.01.
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fig07: HFD and SIRT3 loss reduce capillary density in the heart. Hearts were extracted from WT and KO mice fed ND or HFD for 16 weeks. Ventricular sections were prepared and stained with green fluorescent isolectin B4 (IB4) as an endothelial cell marker. (A) Representative images of mouse hearts from WT-ND, WT-HFD, KO-ND and KO-HFD (a, b, c and d respectively) are shown. (B) IB4 staining was quantified by Image J and normalized to DAPI staining of nuclei (relative intensity). Values are mean ± SEM, n = 3 mice per group. PI, PD and PS ≤ 0.01; *P ≤ 0.05; **P ≤ 0.01. (C) Cell proliferation assay. The proliferation of microvascular endothelial cells from WT and SIRT3 KO lungs was assessed using an MTT assay. Values are mean ± SEM, n = 5 independent observations; **P ≤ 0.01.

Mentions: We next explored whether impairment of HIF-α signalling affected the vasculature of the heart as cardiac dysfunction is associated with decreases in capillary density and coronary blood flow. Wild-type mice fed with HFD showed a marked decrease in capillary density compared to WT mice fed ND (Fig.7A and B). Intriguingly, greater loss of capillary density was observed in SIRT3 KO mice, which was not further enhanced by HFD (PI ≤ 0.01). This finding indicates that SIRT3 loss contributes to the decrease in capillaries seen with HFD. As Figure7C shows, we observed that deletion of SIRT3 markedly reduced proliferation of endothelial cells, which likely contributed to the reduction in capillaries with HFD.


High-fat diet induces cardiac remodelling and dysfunction: assessment of the role played by SIRT3 loss.

Zeng H, Vaka VR, He X, Booz GW, Chen JX - J. Cell. Mol. Med. (2015)

HFD and SIRT3 loss reduce capillary density in the heart. Hearts were extracted from WT and KO mice fed ND or HFD for 16 weeks. Ventricular sections were prepared and stained with green fluorescent isolectin B4 (IB4) as an endothelial cell marker. (A) Representative images of mouse hearts from WT-ND, WT-HFD, KO-ND and KO-HFD (a, b, c and d respectively) are shown. (B) IB4 staining was quantified by Image J and normalized to DAPI staining of nuclei (relative intensity). Values are mean ± SEM, n = 3 mice per group. PI, PD and PS ≤ 0.01; *P ≤ 0.05; **P ≤ 0.01. (C) Cell proliferation assay. The proliferation of microvascular endothelial cells from WT and SIRT3 KO lungs was assessed using an MTT assay. Values are mean ± SEM, n = 5 independent observations; **P ≤ 0.01.
© Copyright Policy - open-access
Related In: Results  -  Collection

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Show All Figures
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fig07: HFD and SIRT3 loss reduce capillary density in the heart. Hearts were extracted from WT and KO mice fed ND or HFD for 16 weeks. Ventricular sections were prepared and stained with green fluorescent isolectin B4 (IB4) as an endothelial cell marker. (A) Representative images of mouse hearts from WT-ND, WT-HFD, KO-ND and KO-HFD (a, b, c and d respectively) are shown. (B) IB4 staining was quantified by Image J and normalized to DAPI staining of nuclei (relative intensity). Values are mean ± SEM, n = 3 mice per group. PI, PD and PS ≤ 0.01; *P ≤ 0.05; **P ≤ 0.01. (C) Cell proliferation assay. The proliferation of microvascular endothelial cells from WT and SIRT3 KO lungs was assessed using an MTT assay. Values are mean ± SEM, n = 5 independent observations; **P ≤ 0.01.
Mentions: We next explored whether impairment of HIF-α signalling affected the vasculature of the heart as cardiac dysfunction is associated with decreases in capillary density and coronary blood flow. Wild-type mice fed with HFD showed a marked decrease in capillary density compared to WT mice fed ND (Fig.7A and B). Intriguingly, greater loss of capillary density was observed in SIRT3 KO mice, which was not further enhanced by HFD (PI ≤ 0.01). This finding indicates that SIRT3 loss contributes to the decrease in capillaries seen with HFD. As Figure7C shows, we observed that deletion of SIRT3 markedly reduced proliferation of endothelial cells, which likely contributed to the reduction in capillaries with HFD.

Bottom Line: HFD resulted in a significant reduction in SIRT3 expression in the heart.SIRT3 KO mice fed HFD showed greater ROS production and a further reduction in cardiac function compared to SIRT3 KO mice on ND.However, HFD did not further reduce capillary density in SIRT3 KO hearts, implicating SIRT3 loss in HFD-induced capillary rarefaction.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology and Toxicology, The University of Mississippi Medical Center, School of Medicine, Jackson, MS, USA.

No MeSH data available.


Related in: MedlinePlus