Apoe Deficient Mice
Mostrando 1-12 de 39 artigos, teses e dissertações.
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1. Alanyl-glutamine attenuates 5-fluorouracil-induced intestinal mucositis in apolipoprotein E-deficient mice
Apolipoprotein E (APOE=gene, apoE=protein) is a known factor regulating the inflammatory response that may have regenerative effects during tissue recovery from injury. We investigated whether apoE deficiency reduces the healing effect of alanyl-glutamine (Ala-Gln) treatment, a recognized gut-trophic nutrient, during tissue recovery after 5-FU-induced int
Braz J Med Biol Res. Publicado em: 28/04/2015
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2. A esplenectomia aumenta as lesões ateroscleróticas em camundongos deficientes em apoproteína E submetidos a uma dieta aterogênica
Atherosclerosis is an inflammatory immune disease associated with lipid accumulation in the intima layer of arteries. The spleen plays an important immune function, but its influence in development of atherosclerosis remains unclear. Evaluation of the role of the spleen in atherosclerosis is justified due to the high frequency of total splenectomies and the
IBICT - Instituto Brasileiro de Informação em Ciência e Tecnologia. Publicado em: 30/08/2011
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3. Avaliação da hiperhomocisteinemia leve na evolução da aterosclerose em camundongos normais, com hemofilia B, deficiencia dos receptores para LDL ou da apolipoproteina E / Evaluation of mild hyperhomocysteinemia in the development of atherosclerosis in normal, hemophiliac B, LDL receptor-deficient or apolipoprotein E-deficient mice
This study evaluated the effect of controlled mild hyperhomocysteinemia (HHcy) in the development of atherosclerosis using normal, apolipoprotein E-deficient (apoE-/-), LDL receptor-deficient (LDLR-/-), or hemophilia B mice. We quantified atherosclerotic lesions at the aortic sinus and analyzed endoplasmic reticulum (RE) stress by western-blot technique. Con
Publicado em: 2008
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4. Liver-directed gene transfer and prolonged expression of three major human ApoE isoforms in ApoE-deficient mice.
Apolipoprotein E (apoE) plays a key role in lipoprotein metabolism and may have other important biological functions. In humans, there are three common, naturally occurring isoforms of apoE that are associated with differences in lipid levels and atherosclerosis. However, the direct in vivo effects of the apoE isoforms on lipoprotein metabolism and atheroscl
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5. Paradoxical enhancement of atherosclerosis by probucol treatment in apolipoprotein E-deficient mice.
Dietary administration of probucol (0.5%, wt/wt) efficiently reduced total plasma cholesterol levels in apolipoprotein E-deficient mice (apoE-/-) by 40%, with decreases in high density lipoprotein (HDL) and apoAI by 70 and 50%, respectively. Paradoxically, however, aortic atherosclerotic plaques in the probucol-treated apoE-/- mice formed more rapidly than i
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6. Activation of PXR induces hypercholesterolemia in wild-type and accelerates atherosclerosis in apoE deficient mice[S]
The nuclear hormone receptor pregnane X receptor (PXR; also called SXR) functions as a xenobiotic sensor to coordinately regulate xenobiotic metabolism via transcriptional regulation of xenobiotic-detoxifying enzymes and transporters. Although many clinically relevant PXR ligands have been shown to affect cholesterol levels, the role of PXR in cholesterol ho
The American Society for Biochemistry and Molecular Biology.
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7. CD36 mRNA and Protein Expression Levels Are Significantly Increased in the Heart and Testis of apoE Deficient Mice in Comparison to Wild Type (C57BL/6)
CD36, an 88kd-adhesion molecule, plays a major role as a scavenging receptor implicated in cellular lipid metabolism. Secretory mammary epithelium, microvasculature endothelium, adipocytes, smooth muscle cells, and platelets express CD36. In addition, CD36 expression is significantly enhanced in macrophages differentiating into foam cells. The effect of path
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8. Roles of thromboxane A2 and prostacyclin in the development of atherosclerosis in apoE-deficient mice
Production of thromboxane (TX) A2 and PG I2/prostacyclin (PGI2) is increased in patients with atherosclerosis. However, their roles in atherogenesis have not been critically defined. To examine this issue, we cross-bred atherosclerosis-prone apoE-deficient mice with mice deficient in either the TXA receptor (TP) or the PGI receptor (IP). Although they showed
American Society for Clinical Investigation.
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9. Deficiency of acyl CoA:cholesterol acyltransferase 2 prevents atherosclerosis in apolipoprotein E-deficient mice
Deficiency of acyl CoA:cholesterol acyltransferase 2 (ACAT2) in mice results in a reduction in cholesterol ester synthesis in the small intestine and liver, which in turn limits intestinal cholesterol absorption, hepatic cholesterol gallstone formation, and the accumulation of cholesterol esters in the plasma lipoproteins. Here we examined the contribution o
The National Academy of Sciences.
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10. Apolipoprotein E deficiency in mice: gene replacement and prevention of atherosclerosis using adenovirus vectors.
Apolipoprotein E (apoE)-deficient mice develop marked hyperlipidemia as well as atherosclerosis and thus are an excellent animal model for evaluating the potential for gene therapy in human genetic dyslipoproteinemias. Recombinant adenovirus containing either human apoE (rAdv.apoE) or the reporter gene luciferase (rAdv.luc) were generated and infused intrave
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11. ANG II infusion promotes abdominal aortic aneurysms independent of increased blood pressure in hypercholesterolemic mice
Infusion of ANG II in hyperlipidemic mice augments atherosclerosis and causes formation of abdominal aortic aneurysms (AAAs). The purpose of this study was to define the contribution of ANG II-induced hypertension to these vascular pathologies. Male apolipoprotein E (apoE)- and LDL receptor (LDLr)-deficient mice were infused with ANG II (1,000 ng·kg−1·mi
American Physiological Society.
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12. Low-dose expression of a human apolipoprotein E transgene in macrophages restores cholesterol efflux capacity of apolipoprotein E-deficient mouse plasma
Apolipoprotein E- (apoE) deficient (E−/−) mice develop severe hyperlipidemia and diffuse atherosclerosis. Low-dose expression of a human apoE3 transgene in macrophages of apoE-deficient mice (E−/−hTgE+/0), which results in about 5% of wild-type apoE plasma levels, did not correct hyperlipidemia but significantly reduced the extent of atherosclerotic
The National Academy of Sciences.