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Titolo:
Mechanism of endothelial dysfunction in apolipoprotein E-deficient mice
Autore:
dUscio, LV; Baker, TA; Mantilla, CB; Smith, L; Weiler, D; Sieck, GC; Katusic, ZS;
Indirizzi:
Mayo Clin & Mayo Fdn, Dept Anesthesiol, Rochester, MN 55905 USA Mayo Clin & Mayo Fdn Rochester MN USA 55905 siol, Rochester, MN 55905 USA Mayo Clin & Mayo Fdn, Dept Mol Pharmacol, Rochester, MN 55905 USA Mayo Clin & Mayo Fdn Rochester MN USA 55905 acol, Rochester, MN 55905 USA Mayo Clin & Mayo Fdn, Dept Expt Therapeut, Rochester, MN 55905 USA Mayo Clin & Mayo Fdn Rochester MN USA 55905 peut, Rochester, MN 55905 USA
Titolo Testata:
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
fascicolo: 6, volume: 21, anno: 2001,
pagine: 1017 - 1022
SICI:
1079-5642(200106)21:6<1017:MOEDIA>2.0.ZU;2-C
Fonte:
ISI
Lingua:
ENG
Soggetto:
NITRIC-OXIDE SYNTHASE; SUPEROXIDE-DISMUTASE; L-ARGININE; HYPERLIPIDEMIC MICE; RELAXING FACTOR; ATHEROSCLEROSIS; RELAXATION; CELLS; HYPERCHOLESTEROLEMIA; EXPRESSION;
Keywords:
endothelium; nitric oxide; superoxide anion; apolipoprotein E; atherosclerosis;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
41
Recensione:
Indirizzi per estratti:
Indirizzo: Katusic, ZS Mayo Clin & Mayo Fdn, Dept Anesthesiol & Mol Pharmacol & Expt Therapeut, 200 1st St SW, Rochester, MN 55905 USA Mayo Clin & Mayo Fdn 200 1st St SW Rochester MN USA 55905 USA
Citazione:
L.V. d'Uscio et al., "Mechanism of endothelial dysfunction in apolipoprotein E-deficient mice", ART THROM V, 21(6), 2001, pp. 1017-1022

Abstract

Endothelium-dependent relaxations mediated by NO are impaired in a mouse model of human atherosclerosis, Our objective was to characterize the mechanisms underlying endothelial dysfunction in aortas of apolipoprotein E (apoE)-deficient mice, treated for 26 to 29 weeks with a lipid-rich Western-typediet. Aortic rings from apoE-deficient mice showed impaired endothelium-dependent relaxations to acetylcholine (10(-9) to 10(-5) mol/L) and Ca2+ ionophore (10(-9) to 10(-6) mol/L) and endothelium-independent relaxations to diethylammonium (Z)-1 -(N,N-diethylamino)diazen-1-ium-1,2-diolate (DEA-NONOate, 10(-10) to 10(-5) mol/L) compared with aortic rings from C57BL/6J mice (P <0.05), By use of confocal microscopy of an oxidative fluorescent probe (dihydroethidium), increased superoxide anion (O-2(-)) production was demonstrated throughout the aortic wall but mainly in smooth muscle cells of apoE-deficient mice. CuZn-superoxide dismutase (SOD) and Mn-SOD protein expressions were unaltered in the aorta exposed to hypercholesterolemia. A cell-permeable SOD mimetic, Mn(III) tetra(4-benzoic acid) porphyrin chloride (10-5 mol/L), reduced O-2(-) production and partially normalized relaxations toacetylcholine and DEA-NONOate in apoE-deficient mice (P <0.05). [C-14]L-Citrulline assay showed a decrease of Ca2+-dependent NOS activity in aortas from apoE-deficient mice compared with C57BL/6J mice (P <0.05), whereas NO synthase protein expression was unchanged. In addition, cGMP levels were significantly reduced in the aortas of apoE-deficient mice (P <0.05). Our results demonstrate that in apoE-deficient mice on a Western-type fat diet, impairment of endothelial function is caused by increased production of O-2(-)and reduced endothelial NO synthase enzyme activity. Thus, chemical inactivation of NO with O-2(-) and reduced biosynthesis of NO are key mechanisms responsible for endothelial dysfunction in aortas of atherosclerotic apoE-deficient mice.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/04/20 alle ore 20:02:51