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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2008-1-24
pubmed:abstractText
The association between increased concentrations of C-reactive protein (CRP) and future cardiovascular events is well established. However, it is currently unclear whether this clinical observation represents an epiphenomenon or whether the pentraxin may actively promote the development of atherosclerosis. Experimental studies with knockout mice with a defect in apolipoprotein E (ApoE(-/-)) have been used to investigate the role of CRP in atherogenesis, but the results obtained have been contradictory so far. Since knockout mice with a defect in low density lipoprotein receptor (LDLR(-/-)) may represent a better model of atherogenesis compared to ApoE(-/-) animals, we undertook experiments to investigate the atherogenic potential of CRP using LDLR(-/-) knockout mice. We crossbred CRP transgenic animals expressing the human CRP pentraxin (huCRP) to LDLR(-/-) mice, fed the resulting double mutants a pro-atherogenic Western type diet (WTD) for four, eight or 12 weeks, respectively, and quantitated atherosclerotic lesion development. Significant differences of lesion size or lesion composition could not be detected between the huCRP-positive LDLR(-/-) mice and the huCRP-negative LDLR(-/-) controls corroborating the contention that CRP does not play a pathogenetic role in early murine atherogenesis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0340-6245
pubmed:author
pubmed:issnType
Print
pubmed:volume
99
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
196-201
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
No effect of C-reactive protein on early atherosclerosis in LDLR-/- / human C-reactive protein transgenic mice.
pubmed:affiliation
Institute of Clinical Chemistry and Laboratory Medicine, Johannes Gutenberg University Mainz, Mainz, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't