Inbred Mice and their Hybrids as an Animal Model for Atherosclerosis Research

Roberts, A; Thompson, J S

doi:10.1007/978-1-4614-4618-7_18

Cited by 69 publications

(25 citation statements)

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“…There fore, cholesterol concentration in the total aorta might not increase much. Elevated concentration of serum cholesterol seems to facilitate lipid deposition in the arterial wall of the inbred mouse (4,5). To produce more severe hypercholesterolemia than in this study, additional treatment such as pro longation of the feeding period, supplemen tation of an antithyroid drug, or alteration of the diet composition should be further examined.…”

Section: Discussionmentioning

confidence: 99%

Cholesterol metabolism in serum and aorta of inbred mice fed a high-cholesterol diet.

et al. 1984

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Abstract-Biochemical characterization of the serum and aorta in inbred C57BL/ 6Cr mice fed a high-cholesterol diet was investigated by determining the total cholesterol (TC) and free cholesterol (FC) levels in serum, high density lipoprotein (HDL) and aorta.Serum lecithin:cholesterol acyltransferase (LCAT) activity was also determined.A modified fluoroenzymatic method for microdetermination of cholesterol was successfully used. TC and FC levels of the aorta in the mice were significantly increased by the high-cholesterol diet. Serum TC and FC levels of mice fed the high-cholesterol diet were increased about 80% and 110%, respectively, compared with the control.On the other hand, both HDL-TC and HDL-FC levels were decreased about 50%. The HDL-TC/serum-TC ratio was markedly decreased, while the atherogenic index was markedly increased with the high-cholesterol diet. LCAT activity was also strikingly decreased.

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Section: Discussionmentioning

confidence: 99%

Cholesterol metabolism in serum and aorta of inbred mice fed a high-cholesterol diet.

et al. 1984

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“…In order for the mice to accept this diet, it had to be gradually mixed in with chow, and still, the mice on this diet did not gain weight normally [10]. Roberts and Thompson subsequently subjected 13 different inbred strains to this diet, of which 10 tolerated the diet sufficiently to get meaningful results [12]. They characterized two of these 10 strains, the C57BR/cdJ strain and the CBA/J strains.…”

Section: Diet-induced Atherosclerosismentioning

confidence: 99%

“…The parental strains were crossed to make F1 progeny, which had intermediate levels of both plasma cholesterol and aortic root lesions. Thus, by studying different inbred strains, they determined that genetic factors were involved in atherosclerosis susceptibility and altered plasma cholesterol levels in response to this atherogenic diet [12]. It was subsequently noted that both strains responded to the atherogenic diet by a decrease in their HDL cholesterol, but a greater HDL reduction was seen in the atherosclerosis susceptible C57BR/cdJ strain [13] Paigen and her colleagues found that this atherogenic diet was associated with morbid respiratory infections, and they modified it by blending it 1:3 with a 10% fat diet to achieve a diet containing 15% fat, 1.25% cholesterol, and 0.5% cholate [14,15], a diet widely used today, and referred to by many researchers as the 'Paigen diet.'…”

Section: Diet-induced Atherosclerosismentioning

confidence: 99%

The emergence of mouse models of atherosclerosis and their relevance to clinical research

Smith

Breslow

1997

Journal of Internal Medicine

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Due to the ability to introduce or mutate genes, the mouse has become the most common experimental animal model for atherosclerosis research. Wildtype mice on a chow diet do not get atherosclerosis. Three ways to induce atherosclerosis in mice are discussed: diet-induced, apoE deficiency-induced, and LDL receptor-deficiency induced. The atherosclerotic lesions in apoE-deficient mice have been well characterized, and they resemble human lesions in their sites of predilection and progression to the fibroproliferative stage. These mouse models of atherosclerosis are being used to identify genes which modify atherosclerosis susceptibility and in the development of antiatherogenic therapies.

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“…When maintained on these diets for several months, certain strains, but not others, developed fatty streak lesions in the proximal aorta. 8 In the early 1980s, several groups characterized lipoproteins in mice and demonstrated significant genetic variations in lipoprotein levels and structures among inbred strains. 9,10 In the mid1980s, Paigen and colleagues (Paigen et al, 11,12 Nishima et al 13 ) modified the original Thompson diet and refined the methods for evaluation of aortic lesions.…”

Section: Mapping Genes For Atherosclerosis In Micementioning

confidence: 99%

Using Mice to Dissect Genetic Factors in Atherosclerosis

Allayee¹,

Ghazalpour²,

Lusis³

2003

ATVB

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Abstract-The genes that contribute to common, complex forms of atherosclerosis remain largely unknown. Genetic studies in humans have, for the most part, focused on identifying genes that predispose to the traditional risk factors, such as lipid levels and blood pressure, but apart from rare, single-gene disorders, there have been few successes to date. The use of mice to dissect the complex genetic etiology of atherosclerosis offers a viable alternative to human studies, because experimental parameters, such as environment, breeding scheme, and detailed phenotyping, can be controlled. Herein we review how mouse genetics can lead to the identification of genes, some of which would otherwise not have been considered as candidates for atherosclerosis, and provide an overview of the prospects for successful gene discovery in the future.

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Inbred Mice and their Hybrids as an Animal Model for Atherosclerosis Research

Cited by 69 publications

References 1 publication

Cholesterol metabolism in serum and aorta of inbred mice fed a high-cholesterol diet.

Cholesterol metabolism in serum and aorta of inbred mice fed a high-cholesterol diet.

The emergence of mouse models of atherosclerosis and their relevance to clinical research

Using Mice to Dissect Genetic Factors in Atherosclerosis

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