Influences of alpha-tocopherol on cholesterol metabolism and fatty streak development in apolipoprotein E-deficient mice fed an atherogenic diet

Peluzio, M.C.G.; Homem, A.P.P.; César, G; Azevedo, G.S.; Amorim, Regina Helena Caldas de; Cara, Denise Carmona; Saliba, H.; Vieira, Eliane; Arantes, Rosa Esteves; Alvarez-Leite, Jacqueline I.

doi:10.1590/s0100-879x2001001200005

Cited by 17 publications

(12 citation statements)

References 30 publications

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“…Similar to that, a 60% decrease of the atherosclerotic lesions as a result of vitamin E supplementation and decreased monocyte chemoattractant protein-1 (MCP-1) expression was measured in ApoE À/À knockout mice fed an atherogenic diet (Peluzio et al, 2001(Peluzio et al, , 2003.…”

Section: Animal Studiessupporting

confidence: 58%

Cellular, molecular and clinical aspects of vitamin E on atherosclerosis prevention

Munteanu¹,

Zingg

2007

Molecular Aspects of Medicine

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Section: Animal Studiessupporting

confidence: 58%

Cellular, molecular and clinical aspects of vitamin E on atherosclerosis prevention

Munteanu¹,

Zingg

2007

Molecular Aspects of Medicine

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“…In the WHHL rabbit model, inhibition of HO-1 by Sn-protoporphyrin IX increased plasma and tissue lipid peroxide levels, and increased atherosclerotic plaque formation (Ishikawa et al 2001a). However, the fact that the antioxidants vitamin E and probucol exhibited a reduction and an increase in atherosclerosis in mouse (Peluzio et al 2001) and rabbit (Zhang et al 1997) models, respectively, but HO inhibition resulted in increased atherosclerotic lesion formation in both species, suggests a role for HO in modulating atherosclerotic lesion formation.…”

Section: Anti-atherogenic Properties Of Ho-1mentioning

confidence: 99%

Protective role of heme oxygenase in the blood vessel wall during atherogenesis

Hoekstra¹,

Godin²,

Cheng³

2004

Biochem. Cell Biol.

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Several lines of evidence suggest that antioxidant processes and (or) endogenous antioxidants inhibit proatherogenic events in the blood vessel wall. Heme oxygenase (HO), which catabolizes heme to biliverdin, carbon monoxide, and catalytic iron, has been shown to have such antioxidative properties. The HO-1 isoform of heme oxygenase is ubiquitous and can be increased several fold by stimuli that induce cellular oxidative stress. Products of the HO reaction have important effects: carbon monoxide is a potent vasodilator, which is thought to play a role in modulation of vascular tone; biliverdin and its by-product bilirubin are potent antioxidants. Although HO induction results in an increase in catalytic free iron release, the enhancement of intracellular ferritin protein through HO-1 has been reported to decrease the cytotoxic effects of iron. Oxidized LDL has been shown to increase HO-1 expression in endothelial and smooth muscle cell cultures, and during atherogenesis. Further evidence of HO-1 expression associated with atherogenesis has been demonstrated in human, murine and rabbit atherosclerotic lesions. Moreover, genetic models of HO deficiency suggest that the actions of HO-1 are important in modulating the severity of atherosclerosis. Recent experiments in gene therapy using the HO gene suggest that interventions aimed at HO in the vessel wall could provide a novel therapeutic approach for the treatment or prevention of atherosclerotic disease.

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“…Atherosclerotic lesions are characterized by progressive accumulation of lipids, macrophages, natural killer (NK) cells, T and B cells, smooth muscle cells, and fibroproliferative elements in the intima of arteries (30). However, hypercholesterolemia and, mainly, high serum levels of low-density lipoprotein (LDL) are considered an absolute prerequisite for lesion establishment.…”

mentioning

confidence: 99%

Infection withToxoplasma gondiiIncreases Atherosclerotic Lesion in ApoE-Deficient Mice

Portugal¹,

Fernandes²,

César³

et al. 2004

Infect Immun

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Toxoplasma gondii is an intracellular protozoan that elicits a potent inflammatory response during the acute phase of infection. Herein, we evaluate whether T. gondii infection alters the natural course of aortic lesions. ApoE knockout mice were infected with T. gondii, and at 5 weeks of infection, serum, feces, and liver cholesterol; aortic lesion size, cellularity, and inflammatory cytokines; and levels of serum nitrite and gamma interferon (IFN-␥) were analyzed. Our results showed that serum cholesterol and atherogenic lipoproteins were reduced after T. gondii infection. The reduction of serum levels of total cholesterol and atherogenic lipoproteins was associated with increases in the aortic lesion area, numbers of inflammatory cells, and expression of monocyte chemoattractant protein 1 and inducible nitric oxide synthase mRNA in the site of lesions as well as elevated concentrations of IFN-␥ and nitrite in sera of T. gondii-infected animals. These results suggest that infection with T. gondii accelerates atherosclerotic development by stimulating the proinflammatory response and oxidative stress, thereby increasing the area of aortic lesion.Atherosclerotic lesions are characterized by progressive accumulation of lipids, macrophages, natural killer (NK) cells, T and B cells, smooth muscle cells, and fibroproliferative elements in the intima of arteries (30). However, hypercholesterolemia and, mainly, high serum levels of low-density lipoprotein (LDL) are considered an absolute prerequisite for lesion establishment. Several genetic and environmental risk factors have been found to contribute to the development of atherosclerosis (2,22,27,33). Among these factors, the immune system is one of the most important. Innate and adaptive immune responses modulate both the rate of lesion progression and composition of atherosclerotic lesions. ApoE knockout (KO) mice crossed into a recombination activating gene (Rag)-deficient background, which lack B and T lymphocytes, had an 80% decrease in the extension of atherosclerotic lesions (32). In addition, crosses of ApoE KO mice with different types of B-or T-cell-deficient mice also decreased atherosclerotic lesions (2,22,40). Inflammatory cytokines and chemokines, such as gamma interferon (IFN-␥), tumor necrosis factor alpha (TNF-␣), TNF-␤, interleukin-12 (IL-12), IL-1␤, and monocyte chemoattractant protein 1 (MCP-1), increase the influx of monocyte into the endothelium, an important step in fatty streak formation (21,24,39). Therefore, atherosclerosis is now considered a chronic inflammatory disease, and systemic infections are thought to play an important role in initiating and/or perpetuating the pathophysiology of aortic lesions. In fact, some studies indicate that bacterial and viral pathogens could be responsible for atherosclerotic development (35). Sunnemark et al. (37) have shown that the combination of an infection of the protozoan parasite Trypanosoma cruzi with an atherogenic diet induced atherosclerotic lesions in the aorta of atherosclerosis-resistant CBA/...

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Influences of alpha-tocopherol on cholesterol metabolism and fatty streak development in apolipoprotein E-deficient mice fed an atherogenic diet

Cited by 17 publications

References 30 publications

Cellular, molecular and clinical aspects of vitamin E on atherosclerosis prevention

Cellular, molecular and clinical aspects of vitamin E on atherosclerosis prevention

Protective role of heme oxygenase in the blood vessel wall during atherogenesis

Infection withToxoplasma gondiiIncreases Atherosclerotic Lesion in ApoE-Deficient Mice

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