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Spontaneous hypercholesterolemia and arterial lesions in mice lacking apolipoprotein E.
TLDR
Apolipoprotein E-deficient mice generated by gene targeting were used to test this hypothesis and to make a mouse model for spontaneous atherosclerosis, with severe yet viable phenotype that should make them valuable for investigating genetic and environmental factors that modify the atherogenic process. Expand
Mice deficient in cystathionine beta-synthase: animal models for mild and severe homocyst(e)inemia.
TLDR
Heterozygous mutants have approximately 50% reduction in cystathionine beta-synthase mRNA and enzyme activity in the liver and have twice normal plasma homocyst(e)ine levels, which are promising for studying the in vivo role of elevated levels of homocysteine in the etiology of cardiovascular diseases. Expand
A role for macrophage scavenger receptors in atherosclerosis and susceptibility to infection
TLDR
It is shown that targeted disruption of the MSR-A gene in mice results in a reduction in the size of atherosclerotic lesions in an animal deficient in apolipoprotein E, indicating that MSr-A may play a part in host defence against pathogens. Expand
Homocysteine-induced endoplasmic reticulum stress causes dysregulation of the cholesterol and triglyceride biosynthetic pathways.
TLDR
It is reported here that homocysteine-induced endoplasmic reticulum (ER) stress activates both the unfolded protein response and the sterol regulatory element-binding proteins (SREBPs) in cultured human hepatocytes as well as vascular endothelial and aortic smooth muscle cells. Expand
Antineutrophil cytoplasmic autoantibodies specific for myeloperoxidase cause glomerulonephritis and vasculitis in mice.
TLDR
This animal model offers strong support for a direct pathogenic role for ANCA IgG in human glomerulonephritis and vasculitis as well as the pathogenic potential of antibodies alone. Expand
Targeted Replacement of the Mouse Apolipoprotein E Gene with the Common Human APOE3 Allele Enhances Diet-induced Hypercholesterolemia and Atherosclerosis*
TLDR
The structural differences between human APOE3 and mouse ApoE proteins are sufficient to cause an increased susceptibility to dietary-induced hypercholesterolemia and atherosclerosis in the 3/3 mice. Expand
The role of natriuretic peptides in cardioprotection.
TLDR
In studies using cultured neonatal myocytes and fibroblasts, exogenous administration of both ANP and ANP antagonists demonstrated that ANP has antihypertrophic and antifibrotic functions, and it is suggested that the intracardiac natriuretic peptides/cGMP system plays a counter-regulatory role against the intrafiltration renin-angiotensin-aldosterone system and TGF-beta mediated pathway. Expand
Dietary cholesterol, rather than liver steatosis, leads to hepatic inflammation in hyperlipidemic mouse models of nonalcoholic steatohepatitis
TLDR
Findings indicate that dietary cholesterol, possibly in the form of modified plasma lipoproteins, is an important risk factor for the progression to hepatic inflammation in diet‐induced NASH. Expand
The two-receptor model of lipoprotein clearance: tests of the hypothesis in "knockout" mice lacking the low density lipoprotein receptor, apolipoprotein E, or both proteins.
TLDR
The observation that apoB-48 increases more dramatically with apoE deficiency than with LDLR deficiency supports the notion that ApoE binds to a second receptor in addition to the LDLR, and is supported by the observation that superimposition of a HDLR deficiency onto an apo E deficiency does not increase hypercholesterolemia beyond the level observed with apOE deficiency alone. Expand
Targeted Deletion of the Ileal Bile Acid Transporter Eliminates Enterohepatic Cycling of Bile Acids in Mice*
TLDR
It is indicated that Slc10a2 is essential for efficient intestinal absorption of bile acids and that alternative absorptive mechanisms are unable to compensate for loss of Slc 10a2 function. Expand
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