ArticleProceedings of the National Academy of Sciences of the United States of America1998
Low density lipoprotein receptor-negative mice expressing human apolipoprotein B-100 develop complex atherosclerotic lesions on a chow diet: no accentuation by apolipoprotein(a).
Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
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Who cites it
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 149 citations in OpenAlex.
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- Hypercholesterolemia Duration and Brain Area Determine Inflammatory Response Intensity and Apoptotic Mediator Activation in Apo ECellular and molecular neurobiology · 2025Article
- A Review onEndocrine, metabolic & immune disorders drug targets · 2025Review
- What Is the Best Experimental Model for Developing Novel Therapeutics in Peripheral Artery Disease?Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- Translating atherosclerosis research from bench to bedside: navigating the barriers for effective preclinical drug discovery.Clinical science (London, England : 1979) · 2022Article
- The History of the WHHL Rabbit, an Animal Model of Familial Hypercholesterolemia (II) - Contribution to the Development and Validation of the Therapeutics for Hypercholesterolemia and Atherosclerosis.Journal of atherosclerosis and thrombosis · 2020Article
- Cerebrovascular Changes and Neurodegeneration Related to Hyperlipidemia: Characteristics of the Human ApoB-100 Transgenic Mice.Current pharmaceutical design · 2020Article
- Impact of atherosclerotic disease on cerebral microvasculature and tissue oxygenation in awake LDLR-/-hApoB+/+ transgenic mice.Neurophotonics · 2019Article
- Modelling of atherosclerosis in genetically modified animals.American journal of translational research · 2019Review
- Atherosclerosis is associated with a decrease in cerebral microvascular blood flow and tissue oxygenation.PloS one · 2019Article
- mTOR drives cerebral blood flow and memory deficits in LDLRJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018Article
- Characterization of Atherosclerosis Formation in a Murine Model of Type IIa Human Familial Hypercholesterolemia.BioMed research international · 2018Article
- Nonclinical Pharmacology/Toxicology Study of AAV8.TBG.mLDLR and AAV8.TBG.hLDLR in a Mouse Model of Homozygous Familial Hypercholesterolemia.Human gene therapy. Clinical development · 2017Article
- Sequential colonization of periodontal pathogens in induction of periodontal disease and atherosclerosis in LDLRnull mice.Pathogens and disease · 2017Article
- Large animal models of cardiovascular disease.Cell biochemistry and function · 2016Review
- Cultured cells of the blood-brain barrier from apolipoprotein B-100 transgenic mice: effects of oxidized low-density lipoprotein treatment.Fluids and barriers of the CNS · 2015Article
- Development of lipoprotein(a) siRNAs for mechanism of action studies in non-human primate models of atherosclerosis.Journal of cardiovascular translational research · 2015Article
- Animal models of atherosclerosis.World journal of clinical cases · 2014Review
- Hybrid FMT-MRI applied to in vivo atherosclerosis imaging.Biomedical optics express · 2014Article
- Biodistribution of AAV8 vectors expressing human low-density lipoprotein receptor in a mouse model of homozygous familial hypercholesterolemia.Human gene therapy. Clinical development · 2013Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
We have generated mice with markedly elevated plasma levels of human low density lipoprotein (LDL) and reduced plasma levels of high density lipoprotein. These mice have no functional LDL receptors [LDLR-/-] and express a human apolipoprotein B-100 (apoB) transgene [Tg(apoB+/+)] with or without an apo(a) transgene [Tg(apoa+/-)]. Twenty animals (10 males and 10 females) of each of the following four genotypes were maintained on a chow diet: (i) LDLR-/-, (ii) LDLR-/-;Tg(apoa+/-), (iii) LDLR-/-;Tg(apoB+/+), and (iv)LDLR-/-;Tg(apoB+/+);Tg(apo+/-). The mice were killed at 6 mo, and the percent area of the aortic intimal surface that stained positive for neutral lipid was quantified. Mean percent areas of lipid staining were not significantly different between the LDLR-/- and LDLR-/-;Tg(apoa+/-) mice (1.0 +/- 0.2% vs. 1.4 +/- 0.3%). However, the LDLR-/-;Tg(apoB+/+) mice had approximately 15-fold greater mean lesion area than the LDLR-/- mice. No significant difference was found in percent lesion area in the LDLR-/-;Tg(apoB+/+) mice whether or not they expressed apo(a) [18.5 +/- 2.5%, without lipoprotein(a), Lp(a), vs. 16.0 +/- 1.7%, with Lp(a)]. Histochemical analyses of the sections from the proximal aorta of LDLR-/-;Tg(apoB+/+) mice revealed large, complex, lipid-laden atherosclerotic lesions that stained intensely with human apoB-100 antibodies. In mice expressing Lp(a), large amounts of apo(a) protein colocalized with apoB-100 in the lesions. We conclude that LDLR-/-; Tg(apoB+/+) mice exhibit accelerated atherosclerosis on a chow diet and thus provide an excellent animal model in which to study atherosclerosis. We found no evidence that apo(a) increased atherosclerosis in this animal model.
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