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Diet intervention reduces uptake of αvβ3 integrin-targeted PET tracer 18F-galacto-RGD in mouse atherosclerotic plaques.
J. Nucl. Cardiol. 19, 775-784 (2012)
Expression of alpha(v)beta(3) integrin has been proposed as a marker for atherosclerotic lesion inflammation. We studied whether diet intervention reduces uptake of alpha(v)beta(3) integrin-targeted positron emission tomography tracer F-18-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 +/- A 0.5 vs 2.3 +/- A 0.8, P = .5). Uptake of F-18-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 F-18-galacto-RGD in the atherosclerotic plaques in the intervention than high-fat group (P = .007). Uptake of F-18-galacto-RGD in plaques correlated with uptake of H-3-deoxyglucose and nuclear density, which was lower in the intervention than high-fat group (P = .01). Flow cytometry demonstrated macrophages expressing alpha(v) and beta(3) integrins in the aorta. Uptake of F-18-galacto-RGD in mouse atherosclerotic lesions was reduced by lipid-lowering diet intervention. Expression of alpha(v)beta(3) integrin is a potential target for evaluation of therapy response in atherosclerosis.
Impact Factor
Scopus SNIP
Web of Science
Times Cited
Times Cited
Scopus
Cited By
Cited By
Altmetric
2.668
1.020
27
27
Anmerkungen
Besondere Publikation
Auf Hompepage verbergern
Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Wissenschaftlicher Artikel
Schlagwörter
Atherosclerosis ; Pet ; Inflammation ; Molecular Imaging ; Vulnerable Plaque; POSITRON-EMISSION-TOMOGRAPHY; ALPHA-V-BETA-3 INTEGRIN; INFLAMMATION; MICE; HYPERCHOLESTEROLEMIA; NANOPARTICLES; ANGIOGENESIS; EXPRESSION; MODEL
Sprache
englisch
Veröffentlichungsjahr
2012
HGF-Berichtsjahr
2012
ISSN (print) / ISBN
1071-3581
e-ISSN
1532-6551
Zeitschrift
Journal of Nuclear Cardiology
Quellenangaben
Band: 19,
Heft: 4,
Seiten: 775-784
Verlag
Springer
Begutachtungsstatus
Peer reviewed
POF Topic(s)
30205 - Bioengineering and Digital Health
30504 - Mechanisms of Genetic and Environmental Influences on Health and Disease
30504 - Mechanisms of Genetic and Environmental Influences on Health and Disease
Forschungsfeld(er)
Enabling and Novel Technologies
PSP-Element(e)
G-500390-001
G-500300-001
G-500300-001
PubMed ID
22527796
WOS ID
WOS:000306342300017
Scopus ID
84865096948
Erfassungsdatum
2012-08-02