http://purl.uniprot.org/citations/17702862 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/17702862 | http://www.w3.org/2000/01/rdf-schema#comment | "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(100/100)Ldlr(-/-)), 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)Apob(100/100)Ldlr(-/-) mice than in hCRP(0/0)Apob(100/100)Ldlr(-/-) 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(+/0)Apob(100/100)Ldlr(-/-) 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(+/0)Apob(100/100)Ldlr(-/-) 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."xsd:string |
http://purl.uniprot.org/citations/17702862 | http://purl.org/dc/terms/identifier | "doi:10.1073/pnas.0706027104"xsd:string |
http://purl.uniprot.org/citations/17702862 | http://purl.uniprot.org/core/author | "Nilsson R."xsd:string |
http://purl.uniprot.org/citations/17702862 | http://purl.uniprot.org/core/author | "Tegner J."xsd:string |
http://purl.uniprot.org/citations/17702862 | http://purl.uniprot.org/core/author | "Kovacs A."xsd:string |
http://purl.uniprot.org/citations/17702862 | http://purl.uniprot.org/core/author | "Hamsten A."xsd:string |
http://purl.uniprot.org/citations/17702862 | http://purl.uniprot.org/core/author | "Bjorkegren J."xsd:string |
http://purl.uniprot.org/citations/17702862 | http://purl.uniprot.org/core/author | "Tornvall P."xsd:string |
http://purl.uniprot.org/citations/17702862 | http://purl.uniprot.org/core/date | "2007"xsd:gYear |
http://purl.uniprot.org/citations/17702862 | http://purl.uniprot.org/core/name | "Proc Natl Acad Sci U S A"xsd:string |
http://purl.uniprot.org/citations/17702862 | http://purl.uniprot.org/core/pages | "13768-13773"xsd:string |
http://purl.uniprot.org/citations/17702862 | http://purl.uniprot.org/core/title | "Human C-reactive protein slows atherosclerosis development in a mouse model with human-like hypercholesterolemia."xsd:string |
http://purl.uniprot.org/citations/17702862 | http://purl.uniprot.org/core/volume | "104"xsd:string |
http://purl.uniprot.org/citations/17702862 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/17702862 |
http://purl.uniprot.org/citations/17702862 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/17702862 |
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