INTERACTION OF LYSOPHOSPHATIDYLCHOLINE WITH AORTIC ENDOTHELIAL-CELLS

被引:25
作者
STOLL, LL
OSKARSSON, HJ
SPECTOR, AA
机构
[1] UNIV IOWA, DEPT BIOCHEM, IOWA CITY, IA 52242 USA
[2] UNIV IOWA, DEPT ANESTHESIA, IOWA CITY, IA 52242 USA
[3] UNIV IOWA, DEPT INTERNAL MED, IOWA CITY, IA 52242 USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY | 1992年 / 262卷 / 06期
关键词
PHOSPHATIDYLCHOLINE; FATTY ACID; LOW-DENSITY LIPOPROTEINS; ALBUMIN; CELL POLARITY; MICROPORE FILTERS; PERMEABILITY; CYTOTOXICITY;
D O I
10.1152/ajpheart.1992.262.6.H1853
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
To better understand the vascular actions of lysophosphatidylcholine (lysoPC), we studied the interaction of [1-C-14]palmitate-labeled lysoPC with bovine aortic endothelial cells. These cells took up lysoPC from media containing albumin, low-density lipoproteins (LDL), or acetyl-LDL. Uptake occurred faster than conversion to phosphatidylcholine (PC), leading to some lysoPC accumulation in endothelial lipids. Endothelial cell monolayers grown on micropore filters took up lysoPC from both apical and basolateral surfaces, preventing substantial amounts from passage across the endothelial monolayer. However, lysoPC present in the interstitial medium of an endothelial-smooth muscle coculture was incorporated primarily by the smooth muscle cells. Endothelial cells grown on filters released lysoPC into both the apical and basolateral medium in the presence of albumin or lipoproteins. Exposure to 50-mu-M lysoPC produced no evidence of endothelial cytotoxicity, but prostaglandin (PG)I2 production was reduced. These studies suggest that the endothelium can participate in the processing of circulating lysoPC and, through basolateral uptake, can facilitate the removal of lysoPC formed within the arterial wall. By decreasing PGI2 output, however, exposure to high concentrations of lysoPC may reduce the antithrombotic and vasodilator capacity of the endothelium.
引用
收藏
页码:H1853 / H1860
页数:8
相关论文
共 22 条
[1]  
ARON L, 1978, J BIOL CHEM, V253, P7220
[2]   DEGRADATION OF CATIONIZED LOW-DENSITY LIPOPROTEIN AND REGULATION OF CHOLESTEROL-METABOLISM IN HOMOZYGOUS FAMILIAL HYPERCHOLESTEROLEMIA FIBROBLASTS [J].
BASU, SK ;
GOLDSTEIN, JL ;
ANDERSON, RGW ;
BROWN, MS .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1976, 73 (09) :3178-3182
[3]   LYSOPHOSPHATIDYLCHOLINE AND SODIUM-CALCIUM EXCHANGE IN CARDIAC SARCOLEMMA - COMPARISON WITH ISCHEMIA [J].
BERSOHN, MM ;
PHILIPSON, KD ;
WEISS, RS .
AMERICAN JOURNAL OF PHYSIOLOGY, 1991, 260 (03) :C433-C438
[4]   THE ROLE OF LYSOLECITHIN IN THE RELAXATION OF VASCULAR SMOOTH-MUSCLE [J].
BING, RJ ;
SAEED, M .
BIOSCIENCE REPORTS, 1987, 7 (10) :783-789
[5]   INTERACTION BETWEEN LIPIDS AND BOVINE BRAIN CALMODULIN - LYSOPHOSPHATIDYLCHOLINE-INDUCED CONFORMATION CHANGE [J].
CHIBA, K ;
KURASHIMA, S ;
MOHRI, T .
LIFE SCIENCES, 1990, 47 (11) :953-960
[6]  
FINE JB, 1982, J LIPID RES, V23, P660
[7]   DISTRIBUTION AND CHEMICAL COMPOSITION OF ULTRACENTRIFUGALLY SEPARATED LIPOPROTEINS IN HUMAN SERUM [J].
HAVEL, RJ ;
EDER, HA ;
BRAGDON, JH .
JOURNAL OF CLINICAL INVESTIGATION, 1955, 34 (09) :1345-1353
[8]   IMPAIRMENT OF ENDOTHELIUM-DEPENDENT ARTERIAL RELAXATION BY LYSOLECITHIN IN MODIFIED LOW-DENSITY LIPOPROTEINS [J].
KUGIYAMA, K ;
KERNS, SA ;
MORRISETT, JD ;
ROBERTS, R ;
HENRY, PD .
NATURE, 1990, 344 (6262) :160-162
[9]   THE ASSOCIATION OF LYSOPHOSPHATIDYLCHOLINE WITH ISOLATED CARDIAC MYOCYTES [J].
MAN, RYK ;
KINNAIRD, AAA ;
BIHLER, I ;
CHOY, PC .
LIPIDS, 1990, 25 (08) :450-454
[10]  
OISHI K, 1988, J BIOL CHEM, V263, P6865