Document Detail


Apolipoprotein E4 domain interaction accelerates diet-induced atherosclerosis in hypomorphic Arg-61 apoe mice.
MedLine Citation:
PMID:  22441102     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: Apolipoprotein (apo) E4 is an established risk factor for atherosclerosis, but the structural components underlying this association remain unclear. ApoE4 is characterized by 2 biophysical properties: domain interaction and molten globule state. Substituting Arg-61 for Thr-61 in mouse apoE introduces domain interaction without molten globule state, allowing us to delineate potential proatherogenic effects of domain interaction in vivo.
METHODS AND RESULTS: We studied atherosclerosis susceptibility of hypomorphic Apoe mice expressing either Thr-61 or Arg-61 apoE (ApoeT(h/h) or ApoeR(h/h)mice). On a chow diet, both mouse models were normolipidemic with similar levels of plasma apoE and lipoproteins. However, on a high-cholesterol diet, ApoeR(h/h) mice displayed increased levels of total plasma cholesterol and very-low-density lipoprotein as well as larger atherosclerotic plaques in the aortic root, arch, and descending aorta compared with ApoeT(h/h) mice. In addition, evidence of cellular dysfunction was identified in peritoneal ApoeR(h/h) macrophages which released lower amounts of apoE in culture medium and displayed increased expression of major histocompatibility complex class II molecules.
CONCLUSIONS: These data indicate that domain interaction mediates proatherogenic effects of apoE4 in part by modulating lipoprotein metabolism and macrophage biology. Pharmaceutical targeting of domain interaction could lead to new treatments for atherosclerosis in apoE4 individuals.
Authors:
Delphine Eberlé; Roy Y Kim; Fu Sang Luk; Nabora Soledad Reyes de Mochel; Nathalie Gaudreault; Victor R Olivas; Nikit Kumar; Jessica M Posada; Andrew C Birkeland; Joseph H Rapp; Robert L Raffai
Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2012-03-22
Journal Detail:
Title:  Arteriosclerosis, thrombosis, and vascular biology     Volume:  32     ISSN:  1524-4636     ISO Abbreviation:  Arterioscler. Thromb. Vasc. Biol.     Publication Date:  2012 May 
Date Detail:
Created Date:  2012-04-20     Completed Date:  2012-07-10     Revised Date:  2013-05-20    
Medline Journal Info:
Nlm Unique ID:  9505803     Medline TA:  Arterioscler Thromb Vasc Biol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1116-23     Citation Subset:  IM    
Affiliation:
Department of Surgery, University of California San Francisco and VA Medical Center, San Francisco, CA 94121, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apolipoprotein E4 / biosynthesis,  genetics*
Atherosclerosis / etiology,  genetics*,  metabolism
DNA / genetics*
Diet, Atherogenic / adverse effects
Disease Models, Animal
Gene Expression Regulation*
Genetic Predisposition to Disease*
Macrophages, Peritoneal / metabolism,  pathology
Mice
Mice, Inbred C57BL
Mice, Knockout
Grant Support
ID/Acronym/Agency:
HL089871/HL/NHLBI NIH HHS; R01 HL089871-01/HL/NHLBI NIH HHS; R01 HL089871-02S1/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Apolipoprotein E4; 9007-49-2/DNA
Comments/Corrections

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