Endothelial Dysfunction in the Apolipoprotein E-deficient Mouse: insights into the influence of diet, gender and aging

@article{Meyrelles2011EndothelialDI,
  title={Endothelial Dysfunction in the Apolipoprotein E-deficient Mouse: insights into the influence of diet, gender and aging},
  author={S. S. Meyrelles and V. Peotta and T. M. Pereira and E. C. Vasquez},
  journal={Lipids in Health and Disease},
  year={2011},
  volume={10},
  pages={211 - 211}
}
Since the early 1990s, several strains of genetically modified mice have been developed as models for experimental atherosclerosis. Among the available models, the apolipoprotein E-deficient (apoE-/-) mouse is of particular relevance because of its propensity to spontaneously develop hypercholesterolemia and atherosclerotic lesions that are similar to those found in humans, even when the mice are fed a chow diet. The main purpose of this review is to highlight the key achievements that have… Expand
Cardiovascular Autonomic Imbalance and Baroreflex Dysfunction in the Apolipoprotein E-deficient Mouse
TLDR
An overview of abnormalities of the parasympathetic and sympathetic nervous systems controlling heart rate and blood pressure and how this dysfunction is influenced by nitric oxide, reactive oxygen species, aging and an atherogenic diet in the apoE-/-mouse is provided. Expand
Sex differences in the development of vascular and renal lesions in mice with a simultaneous deficiency of Apoe and the integrin chain Itga8
TLDR
In this model of atherosclerosis, the female sex is a risk factor to develop more severe atherosclerotic lesions, even though serum fat levels are higher in males, and female mice are protected from renal damage, which is accompanied by attenuated inflammation and matrix deposition. Expand
Chronic iron overload intensifies atherosclerosis in apolipoprotein E deficient mice: Role of oxidative stress and endothelial dysfunction.
TLDR
The results showed that chronic iron overload intensifies the atherosclerotic process and induces endothelial dysfunction in atheosclerotic mice, probably due to the oxidative stress and the imbalance between the relaxing and contractile factors synthesized by the damaged endothelium. Expand
Cardiac and vascular phenotypes in the apolipoprotein E-deficient mouse
TLDR
The apolipoprotein E-deficient mouse has been the most widely used animal model of atherosclerosis because it rapidly develops severe hypercholesterolemia and spontaneous atherosclerotic lesions similar to those observed in humans. Expand
The Concurrence of Hypercholesterolemia and Aging Promotes DNA Damage in Apolipoprotein E-Deficient Mice
TLDR
The novelty of this study is that DNA damage occurring in whole blood cells of this murine model requires the concurrence of aging and oxida- tive stress-related hypercholesterolemia. Expand
Aspirin but not meloxicam attenuates early atherosclerosis in apolipoprotein E knockout mice.
TLDR
It is suggested that low dose aspirin reduces early atherosclerosis, while inhibition of COX-2 by meloxicam is not associated with an increase in atherosclerotic plaque size in this mouse model. Expand
Chronic Cadmium Exposure Accelerates the Development of Atherosclerosis and Induces Vascular Dysfunction in the Aorta of ApoE−/− Mice
TLDR
Cadmium exposure induces endothelial dysfunction, accelerates atherosclerotic plaque formation in the aorta, and enhances oxidative stress in apolipoprotein E knockout (ApoE−/−) mice, and the hypothesis that cadmium Exposure might increase the risk of atherosclerosis is supported. Expand
Thyroid hormone receptor-α deletion decreases heart function and exercise performance in apolipoprotein E-deficient mice.
TLDR
The deletion of TRα in ApoE (-/-)TRα(0/0) mice alters cardiac structure and contractility; both could contribute to blunted BP response to physical exercise and impaired exercise performance. Expand
Sildenafil restores endothelial function in the apolipoprotein E knockout mouse
TLDR
This is the first study demonstrating the beneficial effects of chronic treatment with sildenafil on endothelial dysfunction and atherosclerosis in a model of spontaneous hypercholesterolemia and the main mechanism appears to involve an enhancement of the NO pathway along with a reduction in oxidative stress. Expand
Testing the iron hypothesis in a mouse model of atherosclerosis.
TLDR
It is found that hepatic hepcidin expression was not increased at any stage of the Atherosclerosis progression in Apoe(-/-) or Apoe/ffe mice and that the atherosclerotic plaque size was notincreased in mice with elevated macrophage iron. Expand
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 138 REFERENCES
Endothelial dysfunction of resistance vessels in female apolipoprotein E-deficient mice
TLDR
The endothelial dysfunction in hypercholesterolemic animals was so marked that ovariectomy, which impaired endothelial function in C57 mice, did not cause additional vascular damage in ApoE-deficient mice. Expand
Atherosclerosis in the apolipoprotein-E-deficient mouse: a decade of progress.
TLDR
The apolipoprotein E-deficient mouse is particularly popular because of its propensity to spontaneously develop atherosclerotic lesions on a standard chow diet and some of the nutritional, pharmacological, and genetic studies that have enhanced this understanding. Expand
Plaque-associated endothelial dysfunction in apolipoprotein E-deficient mice on a regular diet. Effect of human apolipoprotein AI.
TLDR
Endothelial dysfunction in apoE(-/-) mice is not affected by hypercholesterolemia alone, but is strictly associated with plaque formation, and ApoAI improved vasomotor responses in atherosclerotic segments. Expand
Hypertension and endothelial dysfunction in apolipoprotein E knockout mice.
Mice lacking ApoE (Apoe(-/-)) develop initially hypercholesterolemia and lastly atherosclerosis. This study examined hemodynamics and endothelial function in 6-week-old Apoe(-/-) mice withExpand
Persistence of the Nitric Oxide Pathway in the Aorta of Hypercholesterolemic Apolipoprotein-E-Deficient Mice
TLDR
The results highlight that ApoE KO mice represent an atypical model of atherosclerosis and could be preserved by upregulation of enzymes involved in redox status such as CuZn or Mn superoxide dismutase and catalase, however, these enzymes were less expressed in Apolipoprotein-E-deficient mice than in control mice. Expand
Chronic ETA receptor blockade prevents endothelial dysfunction of small arteries in apolipoprotein E-deficient mice
TLDR
Severe hypercholesterolemia in apoE-deficient mice is associated with attenuation of NO-mediated relaxation to acetylcholine and increased vascular endothelin-1 content. Expand
Sex as a profound modifier of atherosclerotic lesion development in apolipoprotein E-deficient mice with different genetic backgrounds.
TLDR
The results demonstrate that atherosclerosis-related differences between Ola129 and C57BL/6J genetic backgrounds in apoE-deficient mice are sex-dependent and that this finding is explained by the differences in HDL cholesterol and its apolipoprotein components, mainly apoA-I and A-II. Expand
Inhibition of Diet-Induced Atherosclerosis and Endothelial Dysfunction in Apolipoprotein E/Angiotensin II Type 1A Receptor Double-Knockout Mice
TLDR
Genetic disruption of the AT1A receptor leads to inhibition of vascular oxidative stress, endothelial dysfunction, and atherosclerotic lesion formation in ApoE−/− mice irrespective of blood pressure and plasma cholesterol levels, which indicate a fundamental role of AT1 receptor activation in atherogenesis. Expand
Chronic ET(A) receptor blockade prevents endothelial dysfunction of small arteries in apolipoprotein E-deficient mice.
TLDR
Severe hypercholesterolemia in apoE-deficient mice is associated with attenuation of NO-mediated relaxation to acetylcholine and increased vascular endothelin-1 content. Expand
Mouse models of experimental atherosclerosis.
TLDR
Since 1992 the mouse has become an excellent model for experimental atherosclerosis research, and of the genetically engineered models, the apoE -- deficient model is the only one that develops extensive atherosclerotic lesions on a chow diet. Expand
...
1
2
3
4
5
...