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Human C-reactive protein slows atherosclerosis development in a mouse model with human-like hypercholesterolemia
Atherosclerosis Research group KI.
Cardiology Unit KI.
Linköping University, The Institute of Technology. Linköping University, Department of Physics, Chemistry and Biology, Computational Biology .
Linköping University, The Institute of Technology. Linköping University, Department of Physics, Chemistry and Biology, Computational Biology .
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2007 (English)In: Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, E-ISSN 1091-6490, Vol. 104, no 34, 13768-13773 p.Article in journal (Refereed) Published
Abstract [en]

Increased baseline values of the acute-phase reactant C-reactive protein (CRP) are significantly associated with future cardiovascular disease, and some in vitro studies have claimed that human CRP (hCRP) has proatherogenic effects. In vivo studies in apolipoprotein E-deficient mouse models, however, have given conflicting results. We bred atherosclerosis-prone mice (Apob 100/100Ldlr-/-), which have human-like hypercholesterolemia, with hCRP transgenic mice (hCRP+/0) and studied lesion development at 15, 30, 40, and 50 weeks of age. Atherosclerotic lesions were smaller in hCRP+/0 Apob100/100Ldlr-/- mice than in hCRP0/0Apob100/100Ldlr-/- controls, as judged from the lesion surface areas of pinned-out aortas from mice at 40 and 50 weeks of age. In lesions from 40-week-old mice, mRNA expression levels of several genes in the proteasome degradation pathway were higher in hCRP +/0Apob100/100Ldlr-/- mice than in littermate controls, as shown by global gene expression profiles. These results were confirmed by real-time PCR, which also indicated that the activities of those genes were the same at 30 and 40 weeks in hCRP+/0Apob 100/100Ldlr-/- mice but were significantly lower at 40 weeks than at 30 weeks in controls. Our results show that hCRP is not proatherogenic but instead slows atherogenesis, possibly through proteasome-mediated protein degradation. © 2007 by The National Academy of Sciences of the USA.

Place, publisher, year, edition, pages
2007. Vol. 104, no 34, 13768-13773 p.
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Natural Sciences
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URN: urn:nbn:se:liu:diva-38391DOI: 10.1073/pnas.0706027104Local ID: 44125OAI: oai:DiVA.org:liu-38391DiVA: diva2:259240
Available from: 2009-10-10 Created: 2009-10-10 Last updated: 2017-12-13

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Nilsson, RolandTegnér, Jesper

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