Uptake of 13-hydroperoxylinoleic acid by cultured cells

被引:18
作者
Augé, N [1 ]
Santanam, N [1 ]
Mori, N [1 ]
Keshava, C [1 ]
Parthasarathy, S [1 ]
机构
[1] Emory Univ, Dept Gynecol & Obstet, Atlanta, GA 30322 USA
关键词
atherosclerosis; linoleic acid; 13-hydroperoxyoctadecadienoic acid endothelial cells; macrophages;
D O I
10.1161/01.ATV.19.4.925
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Oxidized free fatty acids have profound effects on cultured cells. However, little is known about whether these effects depend on their uptake and metabolism by cells or primarily involve their interaction with cell-surface components. We determined the uptake and metabolism of unoxidized (linoleic or oleic acid) and oxidized linoleic acid (13-hydroperoxyoctadecadienoic acid, 13-HPODE) by endothelial cells, smooth muscle cells, and macrophages. We show that 13-HPODE is poorly taken up by cells. The levels of uptake were dependent on the cell type but were independent of the expression of CD36. 13-HPODE was also poorly used by microsomal lysophosphatidylcholine acyltransferase that is involved in the formation of phosphatidylcholine. Based on these results, we suggest that most of the biological effects of 13-HPODE and other oxidized free fatty acids on cells might involve a direct interaction with cell-surface components. Alternatively, very small amounts of oxidized free fatty acids that enter the cell may have effects, analogous to those of hormones or prostanoids.
引用
收藏
页码:925 / 931
页数:7
相关论文
共 55 条
[21]   Evidence for human thromboxane receptor heterogeneity using a novel series of 9,11-cyclic carbonate derivatives of prostaglandin F-2 alpha [J].
Krauss, AHP ;
Woodward, DF ;
Gibson, LL ;
Protzman, CE ;
Williams, LS ;
Burk, RM ;
Gac, TS ;
Roof, MB ;
Abbas, F ;
Marshall, K ;
Senior, J .
BRITISH JOURNAL OF PHARMACOLOGY, 1996, 117 (06) :1171-1180
[22]  
KU G, 1992, J BIOL CHEM, V267, P14183
[23]   VASCULAR CELL-ADHESION MOLECULE-1 (VCAM-1) GENE-TRANSCRIPTION AND EXPRESSION ARE REGULATED THROUGH AN ANTIOXIDANT SENSITIVE MECHANISM IN HUMAN VASCULAR ENDOTHELIAL-CELLS [J].
MARUI, N ;
OFFERMANN, MK ;
SWERLICK, R ;
KUNSCH, C ;
ROSEN, CA ;
AHMAD, M ;
ALEXANDER, RW ;
MEDFORD, RM .
JOURNAL OF CLINICAL INVESTIGATION, 1993, 92 (04) :1866-1874
[24]   INCORPORATION OF LIPOXYGENASE PRODUCTS INTO CHOLESTERYL ESTERS BY ACYL-COA - CHOLESTEROL ACYLTRANSFERASE IN CHOLESTEROL-RICH MACROPHAGES [J].
MATHUR, SN ;
ALBRIGHT, E ;
FIELD, FJ .
BIOCHEMICAL JOURNAL, 1988, 256 (03) :807-814
[25]   INCREASED PRODUCTION OF LIPOXYGENASE PRODUCTS BY CHOLESTEROL-RICH MOUSE MACROPHAGES [J].
MATHUR, SN ;
FIELD, FJ ;
SPECTOR, AA ;
ARMSTRONG, ML .
BIOCHIMICA ET BIOPHYSICA ACTA, 1985, 837 (01) :13-19
[26]  
MOWRI H, 1986, BIOCHEM INT, V12, P347
[27]   COMPARATIVE EFFECT OF LIPOXYGENASE PRODUCTS OF ARACHIDONIC-ACID ON RAT AORTIC SMOOTH-MUSCLE CELL-MIGRATION [J].
NAKAO, J ;
OOYAMA, T ;
ITO, H ;
CHANG, WC ;
MUROTA, SI .
ATHEROSCLEROSIS, 1982, 44 (03) :339-342
[28]   ROLE OF THE LIPOXYGENASE PATHWAY IN ANGIOTENSIN-II-INDUCED VASCULAR SMOOTH-MUSCLE CELL HYPERTROPHY [J].
NATARAJAN, R ;
GONZALES, N ;
LANTING, L ;
NADLER, J .
HYPERTENSION, 1994, 23 (01) :I142-I147
[29]   OXIDIZED LDL BINDS TO CD36 ON HUMAN MONOCYTE-DERIVED MACROPHAGES AND TRANSFECTED CELL-LINES - EVIDENCE IMPLICATING THE LIPID MOIETY OF THE LIPOPROTEIN AS THE BINDING-SITE [J].
NICHOLSON, AC ;
FRIEDA, S ;
PEARCE, A ;
SILVERSTEIN, RL .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1995, 15 (02) :269-275
[30]   Role of the lipoxygenase pathway in phenylephrine-induced vascular smooth muscle cell proliferation and migration [J].
Nishio, E ;
Watanabe, Y .
EUROPEAN JOURNAL OF PHARMACOLOGY, 1997, 336 (2-3) :267-273