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Title:

Diet intervention reduces uptake of ?v?3 integrin-targeted PET tracer 18F-galacto-RGD in mouse atherosclerotic plaques.

Document type:
Journal Article
Author(s):
Saraste, A; Laitinen, I; Weidl, E; Wildgruber, M; Weber, AW; Nekolla, SG; Hölzlwimmer, G; Esposito, I; Walch, A; Leppänen, P; Lisinen, I; Luppa, PB; Ylä-Herttuala, S; Wester, HJ; Knuuti, J; Schwaiger, M
Abstract:
Expression of ?(v)?(3) integrin has been proposed as a marker for atherosclerotic lesion inflammation. We studied whether diet intervention reduces uptake of ?(v)?(3) integrin-targeted positron emission tomography tracer (18)F-galacto-RGD in mouse atherosclerotic plaques.Hypercholesterolemic LDLR(-/-) ApoB(100/100) mice on high-fat diet for 4 months were randomized to further 3 months on high-fat diet (high-fat group, n = 8) or regular mouse chow (intervention group, n = 7). Intima-media ratio describing plaque burden was comparable between intervention and high-fat groups (2.0 ± 0.5 vs 2.3 ± 0.8, P = .5). Uptake of (18)F-galacto-RGD in the aorta was lower in the intervention than high-fat group (%ID/g 0.16 vs 0.23, P < .01). Autoradiography showed 35% lower uptake of (18)F-galacto-RGD in the atherosclerotic plaques in the intervention than high-fat group (P = .007). Uptake of (18)F-galacto-RGD in plaques correlated with uptake of (3)H-deoxyglucose and nuclear density, which was lower in the intervention than high-fat group (P = .01). Flow cytometry demonstrated macrophages expressing ?(v) and ?(3) integrins in the aorta.Uptake of (18)F-galacto-RGD in mouse atherosclerotic lesions was reduced by lipid-lowering diet intervention. Expression of ?(v)?(3) integrin is a potential target for evaluation of therapy response in atherosclerosis.
Journal title abbreviation:
J Nucl Cardiol
Year:
2012
Journal volume:
19
Journal issue:
4
Pages contribution:
775-84
Language:
eng
Fulltext / DOI:
doi:10.1007/s12350-012-9554-5
Pubmed ID:
http://view.ncbi.nlm.nih.gov/pubmed/22527796
Print-ISSN:
1071-3581
TUM Institution:
Institut für Allgemeine Pathologie und Pathologische Anatomie; Institut für Klinische Chemie und Pathobiochemie; Klinik und Poliklinik für Nuklearmedizin
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