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http://purl.uniprot.org/citations/18065445http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/18065445http://www.w3.org/2000/01/rdf-schema#comment"

Aims

The role of scavenger receptors in atherogenesis is controversial as a result of conflicting reports and a recent hypothesis suggesting that scavenger receptor absence would enhance the pro-inflammatory, pro-atherogenic milieu. This study addresses the effect of combined absence of scavenger receptors CD36 and SRA I/II on atherosclerosis lesion development in the apolipoprotein E knock-out (apoE degrees ) model.

Methods

We created background-related strains of apoE degrees , scavenger receptor A I/II knock-out (SRA degrees )/apoE degrees , CD36 knock-out (CD36 degrees )/apoE degrees , and CD36 degrees /SRA degrees /apoE degrees mice that were >99% C57Bl/6. Four-week-old mice were fed a Western diet for 12 weeks and were assessed for lesion burden/morphology, risk factors for atherosclerosis, inflammatory mediators, and macrophage function.

Results

There was a 61 and 74% decrease in total aortic lesion area in CD36 degrees /apoE degrees males and females, respectively, compared with apoE degrees controls. The absence of SRA was protective (32% decrease in lesion) in female mice. The combined absence of CD36 and SRA provided no further protection in either gender. Macrophages from mice lacking CD36 had decreased pro-inflammatory characteristics and less migration to a pro-inflammatory stimulus. Plasma levels of cytokines/chemokines showed that CD36 degrees /apoE degrees and CD36 degrees /SRA degrees /apoE degrees mice had a less pro-inflammatory phenotype compared with apoE degrees and SRA degrees /apoE degrees mice. Oblivious mice in the apoE degrees background ruled out potential 'passenger gene' effects in the case of CD36.

Conclusion

These results provide new insights into the pro-atherogenic mechanisms of CD36 by implicating processes other than modified lipoprotein uptake."xsd:string
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http://purl.uniprot.org/citations/18065445http://purl.uniprot.org/core/author"Febbraio M."xsd:string
http://purl.uniprot.org/citations/18065445http://purl.uniprot.org/core/author"Guy E."xsd:string
http://purl.uniprot.org/citations/18065445http://purl.uniprot.org/core/author"Morton R.E."xsd:string
http://purl.uniprot.org/citations/18065445http://purl.uniprot.org/core/author"Kennedy D.J."xsd:string
http://purl.uniprot.org/citations/18065445http://purl.uniprot.org/core/author"Vanegas D."xsd:string
http://purl.uniprot.org/citations/18065445http://purl.uniprot.org/core/author"Kuchibhotla S."xsd:string
http://purl.uniprot.org/citations/18065445http://purl.uniprot.org/core/author"Nimako G."xsd:string
http://purl.uniprot.org/citations/18065445http://purl.uniprot.org/core/date"2008"xsd:gYear
http://purl.uniprot.org/citations/18065445http://purl.uniprot.org/core/name"Cardiovasc Res"xsd:string
http://purl.uniprot.org/citations/18065445http://purl.uniprot.org/core/pages"185-196"xsd:string
http://purl.uniprot.org/citations/18065445http://purl.uniprot.org/core/title"Absence of CD36 protects against atherosclerosis in ApoE knock-out mice with no additional protection provided by absence of scavenger receptor A I/II."xsd:string
http://purl.uniprot.org/citations/18065445http://purl.uniprot.org/core/volume"78"xsd:string
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