Linked Life Data

8241102

Source:http://linkedlifedata.com/resource/pubmed/id/8241102

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
1994-1-4
pubmed:abstractText
The consequences of the lack of apolipoprotein A-I (apoA-I) were evaluated in mice made to lack apoA-I by gene targeting. Inbred strain 129 mice homozygous for the inactive Apoa1 gene and maintained on regular mouse chow had markedly reduced total cholesterol (26% normal) and high-density lipoprotein (HDL) cholesterol (25% normal) levels in their plasma. Their plasma lipoproteins lacked apoA-I and were reduced in all other apolipoproteins but apoE. ApoE comprises about one third of the protein of HDL particles in homozygotes, whereas it is present in only trace amounts in normal HDL. Despite the reduction of HDL cholesterol, no atherosclerotic lesions were observed in any of the homozygous mice evaluated (up to 15 months of age). After being maintained on an atherogenic diet for 4 weeks, total plasma cholesterol of the homozygous mutants increased by 20 mg/dL, while that of normals increased by 60 mg/dL. Mice with mixed 129 and C57BL/6J genetic backgrounds were fed the atherogenic diet for 20 weeks. A small number of foam cells were found attached to the aortic surface in some of the animals, but the extent and occurrence of these depositions were not related to the apoA-I genotype. Our results demonstrate that a lack of apoA-I does not by itself cause atherosclerosis in mice.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1049-8834
pubmed:author
pubmed:issnType
Print
pubmed:volume
13
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1814-21
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Lack of apoA-I is not associated with increased susceptibility to atherosclerosis in mice.
pubmed:affiliation
Department of Pathology, University of North Carolina, Chapel Hill 27599-7525.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.