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Titolo:
Reduced atherosclerotic lesions in mice deficient for total or macrophage-specific expression of scavenger receptor-A
Autore:
Babaev, VR; Gleaves, LA; Carter, KJ; Suzuki, H; Kodama, T; Fazio, S; Linton, MF;
Indirizzi:
Vanderbilt Univ, Med Ctr, Dept Med, Nashville, TN 37232 USA Vanderbilt Univ Nashville TN USA 37232 Dept Med, Nashville, TN 37232 USA Vanderbilt Univ, Med Ctr, Dept Pathol, Nashville, TN 37232 USA Vanderbilt Univ Nashville TN USA 37232 pt Pathol, Nashville, TN 37232 USA Vanderbilt Univ, Med Ctr, Dept Pharmacol, Nashville, TN 37232 USA Vanderbilt Univ Nashville TN USA 37232 Pharmacol, Nashville, TN 37232 USA Univ Tokyo, Dept Mol Biol & Med, Tokyo, Japan Univ Tokyo Tokyo JapanUniv Tokyo, Dept Mol Biol & Med, Tokyo, Japan
Titolo Testata:
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
fascicolo: 12, volume: 20, anno: 2000,
pagine: 2593 - 2599
SICI:
1079-5642(200012)20:12<2593:RALIMD>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
LOW-DENSITY-LIPOPROTEIN; BONE-MARROW TRANSPLANTATION; SMOOTH-MUSCLE CELLS; LDL RECEPTOR; IN-VIVO; MONOCLONAL-ANTIBODY; GENE-EXPRESSION; MESSENGER-RNA; OXIDIZED LDL; PPAR-GAMMA;
Keywords:
atherosclerosis; macrophages; scavenger receptor type A; foam cells formation; fetal liver cell transplantation;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
43
Recensione:
Indirizzi per estratti:
Indirizzo: Babaev, VR Vanderbilt Univ, Sch Med, Dept Cardiovasc Med, 315 Med Res Bldg2, Nashville, TN 37232 USA Vanderbilt Univ 315 Med Res Bldg 2 Nashville TNUSA 37232 2 USA
Citazione:
V.R. Babaev et al., "Reduced atherosclerotic lesions in mice deficient for total or macrophage-specific expression of scavenger receptor-A", ART THROM V, 20(12), 2000, pp. 2593-2599

Abstract

The absence of the scavenger receptor A (SR-A)-I/II has produced variable effects on atherosclerosis in different murine models, Therefore, we examined whether SR-AI/II deficiency affected atherogenesis in C57BL/6 mice, an inbred strain known to be susceptible to diet-induced atherosclerotic lesionformation, and whether the deletion of macrophage SR-AI/II expression would modulate lesion growth in C57BL/6 mice and LDL receptor (LDLR)(-/-) mice. SR-AI/II-deficient (SR-AI/II-/-) female and male mice on the C57BL/6 background were challenged with a butterfat diet for 30 weeks. No differences were detected in plasma lipids between SR-AI/II-/- and SR-AI/II+/+ mice, whereas both female and male SR-AI/II-/- mice had a tremendous reduction (81% to 86%) in lesion area of the proximal aorta compared with SR-AI/II+/+ mice. Next, to analyze the effect of macrophage-specific SR-AI/II deficiency in atherogenesis, female C57BL/6 mice were lethally irradiated, transplanted with SR-AI/II-/- or SR-AI/II+/+ fetal liver cells, and challenged with the butterfat diet for 16 weeks, In a separate experiment, male LDLR-/- mice were reconstituted with SR-AI/II-/- or SR-AI/II+/+ fetal liver cells and challenged with a Western diet for 10 weeks. No significant differences in plasma lipids and lipoprotein profiles were noted between the control and experimental groups in either experiment. SR-AI/II-/--->C57BL/6 mice, however, had a 60% reduction in lesion area of the proximal aorta compared with SR-AI/II+/+ C57BL/6 mice, A similar level of reduction (60%) in lesion area was noted in the proximal aorta and the entire aorta en face of SR-AI/II-/--->LDLR-/- mice compared with SR-AI/II+/+-->LDLR-/- mice. These results demonstrate in vivo that SR-AI/II expression has no impact on plasma lipid levels and that macrophage SR-AI/II contributes significantly to atherosclerotic lesion formation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/12/20 alle ore 16:47:04