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Titolo:
Dietary supplementation with methionine and homocysteine promotes early atherosclerosis but not plaque rupture in apoE-deficient mice
Autore:
Zhou, J; Moller, J; Danielsen, CC; Bentzon, J; Ravn, HB; Austin, RC; Falk, E;
Indirizzi:
Aarhus Univ Hosp Skejby, Dept Cardiol, DK-8200 Aarhus N, Denmark Aarhus Univ Hosp Skejby Aarhus Denmark N diol, DK-8200 Aarhus N, Denmark Aarhus Univ Hosp Skejby, Dept Clin Biochem, DK-8200 Aarhus, Denmark AarhusUniv Hosp Skejby Aarhus Denmark DK-8200 , DK-8200 Aarhus, Denmark Aarhus Univ Hosp Skejby, Inst Expt Clin Res, DK-8200 Aarhus N, Denmark Aarhus Univ Hosp Skejby Aarhus Denmark N Res, DK-8200 Aarhus N, Denmark Aarhus Univ, Inst Anat, Dept Connect Tissue Biol, Aarhus, Denmark Aarhus Univ Aarhus Denmark t, Dept Connect Tissue Biol, Aarhus, Denmark McMaster Univ, Hamilton, ON, Canada McMaster Univ Hamilton ON CanadaMcMaster Univ, Hamilton, ON, Canada Hamilton Civ Hosp, Res Ctr, Hamilton, ON, Canada Hamilton Civ Hosp Hamilton ON Canada Hosp, Res Ctr, Hamilton, ON, Canada
Titolo Testata:
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
fascicolo: 9, volume: 21, anno: 2001,
pagine: 1470 - 1476
SICI:
1079-5642(200109)21:9<1470:DSWMAH>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
SMOOTH-MUSCLE CELLS; LYSYL OXIDASE; QUANTITATIVE ASSESSMENT; PLASMA HOMOCYSTEINE; ENDOTHELIAL-CELLS; FOLATE-DEFICIENCY; VASCULAR-DISEASE; RISK FACTOR; RATS; HYPERHOMOCYSTEINEMIA;
Keywords:
apoE-deficient mouse; homocysteine; atherosclerosis; plaque rupture;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
38
Recensione:
Indirizzi per estratti:
Indirizzo: Falk, E Aarhus Univ Hosp Skejby, Dept Cardiol Res, DK-8200 Aarhus N, Denmark Aarhus Univ Hosp Skejby Aarhus Denmark N -8200 Aarhus N, Denmark
Citazione:
J. Zhou et al., "Dietary supplementation with methionine and homocysteine promotes early atherosclerosis but not plaque rupture in apoE-deficient mice", ART THROM V, 21(9), 2001, pp. 1470-1476

Abstract

Hyperhomocysteinemia is an independent risk factor for atherothrombosis. However, causality is unproven, and it remains unknown whether hyperhomocysteinemia promotes atherosclerosis, plaque rupture, and/or thrombosis. We evaluated the short- and long-term effects of hyperhomocysteinemia on plaque size and structure in 99 atherosclerosis-prone apolipoprotein E-deficient mice. Hyperhomocysteinemia was induced by methionine (Met) or homocysteine (HcyH) supplementation: low Met (+11 g Met/kg food), high Met (+33 g Met/kg food), low HcyH (0.9 g HcyH/L drinking water), and high HcyH (1.8 g HcyH/L drinking water). Met and HcyH supplementation significantly raised plasma total homocysteine levels by 4- to 16-fold above those observed in mice fed acontrol diet (up to 146.1 mu mol/L). Compared with controls, aortic root plaque size was significantly larger in supplemented groups after 3 months (56% and 173% larger in high-Met and high-HcyH, respectively) but not after 12 months. Hyperhomocysteinemia was associated with an increase in the amount of collagen in plaques after both 3 and 12 months. Mechanical testing ofthe tail tendons revealed no weakening of collagen after 12 months of hyperhomocysteinemia. Many plaques in both control and supplemented mice appeared rupture prone morphologically, but all aortic root plaques and all but 1coronary plaque had an intact surface without rupture or thrombosis. Thus,diet-induced hyperhomocysteinemia promotes early atherosclerosis and plaque fibrosis but does not, even in the long term, weaken collagen or induce plaque rupture.

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Documento generato il 05/04/20 alle ore 07:11:58