Document Detail


Four strains of spontaneously hyperlipidemic (SHL) mice: phenotypic distinctions determined by genetic backgrounds.
MedLine Citation:
PMID:  11866033     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Spontaneously hyperlipidemic (SHL) mice are Japanese wild mice (KOR) with disruption of the apolipoprotein E (Apo E) gene. These mice (KOR-Apoe(shl)) are superhypercholesterolemic and develop severe xanthoma, but their atherosclerosis is relatively mild compared with Apo E knockout mice. First, we tested whether this distinction is due to additional mutation of the Apoc1 and/or Apoc2 genes in KOR-Apoe(shl). Southern blot analysis, but found no gross disruption of these genes. Next, we tested whether the phenotypic distinction is due to differences in the genetic background. To this end, we established three lines of congenic SHL mice with a genetic background of C57BL/6, BALB/c or C3H/He, and named them, respectively, C57BL/6.KOR-Apoe(shl) (B6.KOR-Apoe(shl)), BALB/c.KOR-Apoe(shl) (C.KOR-Apoe(shl)) and C3H/He.KOR-Apoe(shl) (C3.KOR-Apoe(shl)). Hypercholesterolemia was most severe in KOR-Apoe(shl) followed the by others as follows; KOR-Apoe(shl)>>C3.KOR-Apoe(shl)>C.KOR-Apoe(shl)>B6.KOR-Apoe(shl). In contrast, atherosclerosis was most severe in B6.KOR Apoe(shl) followed by the others: B6.KOR-Apoe(shl)>C.KOR-Apoe(shl)>>C3.KOR-Apoe(shl)> or =KOR-Apoe(shl). This order, however, did not match that in xanthoma, which was highly prominent in KOR-Apoe(shl) but mild in B6.KOR-Apoe(shl), C.KOR-Apoe(shl) and C3.KORApoe(shl). This order, however, did not match that in xanthoma, which was highly prominant in KOR-Apoe(shl) but mild in B6.KOR-Apoe(shl), C.KOR-Apoe(shl) and C3.KOR-Apoe(shl). These distinctions suggest that the severity of each of the phenotypes is determined by distinct genetic backgrounds which probably are composed of polymorphism of lipid metabolism-related proteins. We found that apolipoprotein A-I is decreased in each SHL strain and polymorphic between B6.KOR-Apoe(shl) and the other strains examined. This polymorphism may be related to the most severe atherosclerosis observed in B6.KOR-Apoe(shl). It is most likely that combination of such polymorphisms is due to the genetic background accountable for phenotype distinctions.
Authors:
Y Matsushima; T Sakurai; A Ohoka; T Ohnuki; N Tada; Y Asoh; M Tachibana
Related Documents :
21197883 - Engaging physicians in cme: the power of theater.
21411473 - Validation of a job satisfaction scale in the australian clinical medical workforce.
457923 - Patients' understanding of prescribed drugs.
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of atherosclerosis and thrombosis     Volume:  8     ISSN:  1340-3478     ISO Abbreviation:  J. Atheroscler. Thromb.     Publication Date:  2001  
Date Detail:
Created Date:  2002-02-27     Completed Date:  2002-08-20     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  9506298     Medline TA:  J Atheroscler Thromb     Country:  Japan    
Other Details:
Languages:  eng     Pagination:  71-9     Citation Subset:  IM    
Affiliation:
Research Institute, Saitama Cancer Center, Ina, Japan. matsu@cancer-c.pref.saitama.jp
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Arteriosclerosis / genetics,  pathology
Blotting, Southern
Blotting, Western
Cholesterol / blood
Hyperlipidemias / genetics*
Lipoproteins / classification
Mice
Mice, Mutant Strains / genetics*
Phenotype
Species Specificity
Xanthomatosis / genetics,  pathology
Chemical
Reg. No./Substance:
0/Lipoproteins; 57-88-5/Cholesterol

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Heme oxygenase as an intrinsic defense system in vascular wall: implication against atherogenesis.
Next Document:  No association found between the Ala54Thr polymorphism of FABP2 gene and obesity and obesity with dy...