Lipoxygenases and atherosclerosis: Protection versus pathogenesis

被引:90
作者
Cathcart, MK [1 ]
Folcik, VA [1 ]
机构
[1] Cleveland Clin Fdn, Lerner Res Inst, Dept Cell Biol NC10, Cleveland, OH 44195 USA
关键词
atherosclerosis; lipoxygenase; lipid oxidation; inflammation; cytokines; lipoprotein oxidation; monocyte-macrophage activation; free radical; interleukin; 13;
D O I
10.1016/S0891-5849(00)00230-6
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
15 lipoxygenase (15LO) is a lipid-oxidizing enzyme that is considered to contribute to the formation of oxidized lipids in atherosclerotic lesions. Monocyte-macrophages are the key cells that express 15LO in atherosclerotic lesions. In this review, we examine the evidence for 15LO involvement in atherogenesis and explore and evaluate the potential mechanisms whereby 15LO may contribute to the oxidation of LDL by monocyte-macrophages. We also describe several possible pro- versus anti-atherogenic functions that may be mediated by various products of 15LO lipid oxidation. Central pathways involved in regulating 15LO expression and activity that may serve as future targets for intervention and regulation of this enzyme are also reviewed. (C) 2000 Elsevier Science Inc.
引用
收藏
页码:1726 / 1734
页数:9
相关论文
共 73 条
[51]  
RANKIN SM, 1991, J LIPID RES, V32, P449
[52]   LINOLEIC-ACID AND ITS METABOLITES, HYDROPEROXYOCTADECADIENOIC ACIDS, STIMULATE C-FOS, C-JUN, AND C-MYC MESSENGER-RNA EXPRESSION, MITOGEN-ACTIVATED PROTEIN-KINASE ACTIVATION, AND GROWTH IN RAT AORTIC SMOOTH-MUSCLE CELLS [J].
RAO, GN ;
ALEXANDER, RW ;
RUNGE, MS .
JOURNAL OF CLINICAL INVESTIGATION, 1995, 96 (02) :842-847
[53]   THE MATURATIONAL BREAKDOWN OF MITOCHONDRIA IN RETICULOCYTES [J].
RAPOPORT, SM ;
SCHEWE, T .
BIOCHIMICA ET BIOPHYSICA ACTA, 1986, 864 (3-4) :471-495
[54]   Induction of 15-lipoxygenase expression by IL-13 requires tyrosine phosphorylation of Jak2 and Tyk2 in human monocytes [J].
Roy, B ;
Cathcart, MK .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (48) :32023-32029
[55]   LIPID HYDROPEROXIDE-INDUCED APOPTOSIS - LACK OF INHIBITION BY BCL-2 OVER-EXPRESSION [J].
SANDSTROM, PA ;
PARDI, D ;
TEBBEY, PW ;
DUDEK, RW ;
TERRIAN, DM ;
FOLKS, TM ;
BUTTKE, TM .
FEBS LETTERS, 1995, 365 (01) :66-70
[56]   Attenuation of diet-induced atherosclerosis in rabbits with a highly selective 15-lipoxygenase inhibitor lacking significant antioxidant properties [J].
Sendobry, SM ;
Cornicelli, JA ;
Welch, K ;
Bocan, T ;
Tait, B ;
Trivedi, BK ;
Colbry, N ;
Dyer, RD ;
Feinmark, SJ ;
Daugherty, A .
BRITISH JOURNAL OF PHARMACOLOGY, 1997, 120 (07) :1199-1206
[57]   Macrophage-mediated 15-lipoxygenase expression protects against atherosclerosis development [J].
Shen, JH ;
Herderick, E ;
Cornhill, JF ;
Zsigmond, E ;
Kim, HS ;
Kuhn, H ;
Guevara, NV ;
Chan, L .
JOURNAL OF CLINICAL INVESTIGATION, 1996, 98 (10) :2201-2208
[58]   Fibroblasts that overexpress 15-lipoxygenase generate bioactive and minimally modified LDL [J].
Sigari, F ;
Lee, C ;
Witztum, JL ;
Reaven, PD .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1997, 17 (12) :3639-3645
[59]   THE INDUCED LIPOXYGENASE IN ATHEROSCLEROTIC AORTA CONVERTS LINOLEIC-ACID TO THE PLATELET CHEMOREPELLANT FACTOR-13-HODE [J].
SIMON, TC ;
MAKHEJA, AN ;
BAILEY, JM .
THROMBOSIS RESEARCH, 1989, 55 (02) :171-178
[60]   CELLULAR OXIDATIVE MODIFICATION OF LOW-DENSITY-LIPOPROTEIN DOES NOT REQUIRE LIPOXYGENASES [J].
SPARROW, CP ;
OLSZEWSKI, J .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1992, 89 (01) :128-131