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Increased atherosclerosis in mice reconstituted with apolipoprotein E null macrophages

Increased atherosclerosis in mice reconstituted with apolipoprotein E null macrophages

http://www.wikidata.org/entity/Q36143345

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LXRs control lipid-inducible expression of the apolipoprotein E gene in macrophages and adipocytes Atherosclerosis Lack of macrophage fatty-acid-binding protein aP2 protects mice deficient in apolipoprotein E against atherosclerosis Regulated expression of the apolipoprotein E/C-I/C-IV/C-II gene cluster in murine and human macrophages. A critical role for nuclear liver X receptors alpha and beta Increased atherosclerosis in LDL receptor-null mice lacking ACAT1 in macrophages Monocyte/macrophage expression of ABCA1 has minimal contribution to plasma HDL levels Macrophage lipoprotein lipase promotes foam cell formation and atherosclerosis in low density lipoprotein receptor-deficient mice Defining the atherogenicity of large and small lipoproteins containing apolipoprotein B100 Augmented atherogenesis in LDL receptor deficient mice lacking both macrophage ABCA1 and ApoE Genes within the MHC region have a dramatic influence on radiation-enhanced atherosclerosis in mice Reduction of isoprostanes and regression of advanced atherosclerosis by apolipoprotein E.ApoE plasma levels and risk of cardiovascular mortality in old age Adipocyte fatty acid-binding protein, aP2, alters late atherosclerotic lesion formation in severe hypercholesterolemia Macrophage LRP-1 controls plaque cellularity by regulating efferocytosis and Akt activation.Macrophage Apoptosis and Efferocytosis in the Pathogenesis of Atherosclerosis Macrophage lipoprotein lipase promotes foam cell formation and atherosclerosis in vivo Anti-inflammatory effects of tetradecylthioacetic acid (TTA) in macrophage-like cells from Atlantic salmon (Salmo salar L.).Combined vitamin C and vitamin E deficiency worsens early atherosclerosis in apolipoprotein E-deficient mice.Anti-inflammatory and cholesterol-reducing properties of apolipoprotein mimetics: a review Macrophage-derived apoESendai suppresses atherosclerosis while causing lipoprotein glomerulopathy in hyperlipidemic mice.Macrophage-specific apoE gene repair reduces diet-induced hyperlipidemia and atherosclerosis in hypomorphic Apoe mice Conditional disruption of the peroxisome proliferator-activated receptor gamma gene in mice results in lowered expression of ABCA1, ABCG1, and apoE in macrophages and reduced cholesterol efflux.Selective macrophage ascorbate deficiency suppresses early atherosclerosis.Local effects of human PCSK9 on the atherosclerotic lesion.Proteomic identification of biomarkers of vascular injury.Tie1 attenuation reduces murine atherosclerosis in a dose-dependent and shear stress-specific manner Macrophage apoAI protects against dyslipidemia-induced dermatitis and atherosclerosis without affecting HDL.ApoE regulates hematopoietic stem cell proliferation, monocytosis, and monocyte accumulation in atherosclerotic lesions in mice.The combination of high-fat diet-induced obesity and chronic ulcerative colitis reciprocally exacerbates adipose tissue and colon inflammation ApoE suppresses atherosclerosis by reducing lipid accumulation in circulating monocytes and the expression of inflammatory molecules on monocytes and vascular endothelium Atherosclerotic lesions grow through recruitment and proliferation of circulating monocytes in a murine model Apolipoprotein E enhances microRNA-146a in monocytes and macrophages to suppress nuclear factor-κB-driven inflammation and atherosclerosis.Animal models of atherosclerosis.Differential action of glucocorticoids on apolipoprotein E gene expression in macrophages and hepatocytes.Lipoprotein receptors--an evolutionarily ancient multifunctional receptor family.Apolipoprotein E induces antiinflammatory phenotype in macrophages Low-dose expression of a human apolipoprotein E transgene in macrophages restores cholesterol efflux capacity of apolipoprotein E-deficient mouse plasma Absence of regulated splicing of fibronectin EDA exon reduces atherosclerosis in mice.Infection induces a positive acute phase apolipoprotein E response from a negative acute phase gene: role of hepatic LDL receptors.Leishmania major Self-Limited Infection Increases Blood Cholesterol and Promotes Atherosclerosis Development

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P2860

Increased atherosclerosis in mice reconstituted with apolipoprotein E null macrophages

http://www.wikidata.org/entity/Q36143345

description

1997 nî lūn-bûn

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1997年の論文

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1997年論文

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1997年論文

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1997年論文

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1997年論文

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1997年論文

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1997年论文

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1997年论文

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1997年论文

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name

Increased atherosclerosis in mice reconstituted with apolipoprotein E null macrophages

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Increased atherosclerosis in mice reconstituted with apolipoprotein E null macrophages

@en

type

label

Increased atherosclerosis in mice reconstituted with apolipoprotein E null macrophages

@ast

Increased atherosclerosis in mice reconstituted with apolipoprotein E null macrophages

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prefLabel

Increased atherosclerosis in mice reconstituted with apolipoprotein E null macrophages

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Increased atherosclerosis in mice reconstituted with apolipoprotein E null macrophages

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Proceedings of the National Academy of Sciences of the United States of America

P1476

Increased atherosclerosis in mice reconstituted with apolipoprotein E null macrophages

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P2093

A B Murray

http://www.w3.org/2001/XMLSchema#string

J B Atkinson

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K J Carter

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L A Gleaves

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M F Linton

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S Fazio

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V R Babaev

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P2860

The LDL-receptor-related protein, LRP, is an apolipoprotein E-binding protein

Isolation of biologically active ribonucleic acid from sources enriched in ribonuclease

Apolipoprotein E: cholesterol transport protein with expanding role in cell biology

The pathogenesis of atherosclerosis: a perspective for the 1990s

Spontaneous hypercholesterolemia and arterial lesions in mice lacking apolipoprotein E

Promoter traps in embryonic stem cells: a genetic screen to identify and mutate developmental genes in mice

Fluorescence-activated cell analysis and sorting of viable mammalian cells based on beta-D-galactosidase activity after transduction of Escherichia coli lacZ

Type III hyperlipoproteinemic phenotype in transgenic mice expressing dysfunctional apolipoprotein E.

Perivascular microglial cells of the CNS are bone marrow-derived and present antigen in vivo.

Inhibition of diet-induced atheroma formation in transgenic mice expressing apolipoprotein E in the arterial wall.

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9

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94

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Alyssa H. Hasty

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14104210

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9114045

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atherosclerosis

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20778

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