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Titolo:
Disruption of the 12/15-lipoxygenase gene diminishes atherosclerosis in apo E-deficient mice
Autore:
Cyrus, T; Witztum, JL; Rader, DJ; Tangirala, R; Fazio, S; Linton, MF; Funk, CD;
Indirizzi:
Univ Penn, Ctr Expt Therapeut, Philadelphia, PA 19104 USA Univ Penn Philadelphia PA USA 19104 Therapeut, Philadelphia, PA 19104 USA Univ Calif San Diego, Dept Med, La Jolla, CA 92093 USA Univ Calif San Diego La Jolla CA USA 92093 pt Med, La Jolla, CA 92093 USA Univ Penn, Dept Med, Div Cardiovasc Med, Philadelphia, PA 19104 USA Univ Penn Philadelphia PA USA 19104 ovasc Med, Philadelphia, PA 19104 USA Vanderbilt Univ, Sch Med, Dept Med, Div Endocrinol & Diabet, Nashville, TN37232 USA Vanderbilt Univ Nashville TN USA 37232 l & Diabet, Nashville, TN37232 USA
Titolo Testata:
JOURNAL OF CLINICAL INVESTIGATION
fascicolo: 11, volume: 103, anno: 1999,
pagine: 1597 - 1604
SICI:
0021-9738(199906)103:11<1597:DOT1GD>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
LOW-DENSITY-LIPOPROTEIN; SMOOTH-MUSCLE CELLS; 15-LIPOXYGENASE MESSENGER-RNA; LIPID-PROTEIN ADDUCTS; OXIDATIVE MODIFICATION; ENDOTHELIAL-CELLS; APOLIPOPROTEIN-E; OXIDIZED LDL; OVEREXPRESS 15-LIPOXYGENASE; MAMMALIAN LIPOXYGENASES;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
61
Recensione:
Indirizzi per estratti:
Indirizzo: Funk, CD Univ Penn, Ctr Expt Therapeut, 422 Curie Blvd,Room 806, Philadelphia, PA 19104 USA Univ Penn 422 Curie Blvd,Room 806 Philadelphia PA USA 19104 4 USA
Citazione:
T. Cyrus et al., "Disruption of the 12/15-lipoxygenase gene diminishes atherosclerosis in apo E-deficient mice", J CLIN INV, 103(11), 1999, pp. 1597-1604

Abstract

Atherosclerosis may be viewed as an inflammatory disease process that includes early oxidative modification of LDLs, leading to foam cell formation. This "oxidation hypothesis" has gained general acceptance in recent years, and evidence for the role of lipoxygenases in initiation of, or participation in, the oxidative process is accumulating. However, the relative contribution of macrophage-expressed lipoxygenases to atherogenesis in vivo remains unknown. Here, we provide in vivo evidence for the role of 12/15-lipoxygenase in atherogenesis and demonstrate diminished plasma IgG autoantibodies to oxidized LDL epitopes in 12/15-lipoxygenase knockout mice crossbred withatherosclerosis-prone apo E-deficient mice (apo E-/-/L-12LO(-/-)). In chow-fed 15-week-old apo E-/-/L-12LO(-/-) mice, the extent of lesions in whole-aorta en face preparations (198 +/- 60 mu m(2)) was strongly reduced (P < 0.001, n = 12) when compared with 12/15-lipoxygenase-expressing controls (apo E-/-/L-12LO(+/+)), which showed areas of lipid deposition (15,700 +/- 2,688 mu m(2)) in the lesser curvature of the aortic arch, branch points, and in the abdominal aorta. These results were observed despite cholesterol, triglyceride, and lipoprotein levels that were similar to those in apo E-deficient mice. Evidence for reduced lesion development was observed even at 1 year of age in apo E-/-/L-12LO(-/-) mice. The combined data indicate a rolefor 12/15-lipoxygenase in the pathogenesis of atherosclerosis and suggest that inhibition of this enzyme may decrease disease progression.

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Documento generato il 04/12/20 alle ore 06:35:09