Apolipoprotein E Deficiency Increases Remnant Lipoproteins and Accelerates Progressive Atherosclerosis, But Not Xanthoma Formation, in Gene-Modified Minipigs

Deficiency of apolipoprotein E (APOE) causes familial dysbetalipoproteinemia in humans resulting in a higher risk of atherosclerotic disease. In mice, APOE deficiency results in a severe atherosclerosis phenotype, but it is unknown to what extent this is unique to mice. In this study, APOE was targe...

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Detalles Bibliográficos
Autores principales: Shim, Jeong, Poulsen, Christian Bo, Hagensen, Mette K., Larsen, Torben, Heegaard, Peter M.H., Christoffersen, Christina, Bolund, Lars, Schmidt, Mette, Liu, Ying, Li, Juan, Li, Rong, Callesen, Henrik, Bentzon, Jacob F., Sørensen, Charlotte B.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2017
Materias:
PRECLINICAL RESEARCH
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6058916/
https://www.ncbi.nlm.nih.gov/pubmed/30062172
http://dx.doi.org/10.1016/j.jacbts.2017.06.004
Descripción
Sumario:Deficiency of apolipoprotein E (APOE) causes familial dysbetalipoproteinemia in humans resulting in a higher risk of atherosclerotic disease. In mice, APOE deficiency results in a severe atherosclerosis phenotype, but it is unknown to what extent this is unique to mice. In this study, APOE was targeted in Yucatan minipigs. APOE(−/−) minipigs displayed increased plasma cholesterol and accumulation of apolipoprotein B-48–containing chylomicron remnants on low-fat diet, which was significantly accentuated upon feeding a high-fat, high-cholesterol diet. APOE(−/−) minipigs displayed accelerated progressive atherosclerosis but not xanthoma formation. This indicates that remnant lipoproteinemia does not induce early lesions but is atherogenic in pre-existing atherosclerosis.

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