Lysophosphatidylcholine activates mitogen-activated protein kinases by a tyrosine kinase-dependent pathway in bovine aortic endothelial cells

被引：36

作者：

Ozaki, H ^{[1
]}

Ishii, K ^{[1
]}

Arai, H ^{[1
]}

Kume, N ^{[1
]}

Kita, T ^{[1
]}

机构：

[1] Kyoto Univ, Dept Geriatr Med, Grad Sch Med, Sakyo Ku, Kyoto 6068397, Japan

来源：

ATHEROSCLEROSIS | 1999年 / 143卷 / 02期

关键词：

lysophosphatidylcholine; extracellular signal-regulated protein kinase; cJun N-terminal protein kinase; tyrosine kinase;

D O I：

10.1016/S0021-9150(98)00297-4

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Lysophosphatidylcholine (lyso-PC) is a major component of an atherogenic lipoprotein. In this study, to investigate the involvement of mitogen-activated protein kinases in the signaling pathway by lyse-PC in endothelial cells, we measured the activity of extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) in bovine aortic endothelial cells. Lyse-PC activated ERK and JNK in a dose-dependent manner. However, the time courses of activation of these kinases were different. ERK and JNK activation by lyse-PC was inhibited by a tyrosine kinase inhibitor, herbimycin A, but not by a protein kinase C (PKC) specific inhibitor. We conclude, therefore, that lyse-PC-mediated ERK and JNK activation is caused by a tyrosine kinase-dependent mechanism, but not conventional types of PKC-dependent mechanisms. (C) 1999 Elsevier Science Ireland Ltd. All rights reserved.

引用

页码：261 / 266

页数：6

共 41 条

[1] Oxidized low density lipoprotein and lysophosphatidylcholine stimulate cell cycle entry in vascular smooth muscle cells - Evidence for release of fibroblast growth factor-2 [J].

Chai, YC ;

Howe, PH ;

DiCorleto, PE ;

Chisolm, GM .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1996, 271 (30) :17791-17797

[2] LYSOPHOSPHATIDYLCHOLINE CAUSES CA2+ INFLUX, ENHANCED DNA-SYNTHESIS AND CYTOTOXICITY IN CULTURED VASCULAR SMOOTH-MUSCLE CELLS [J].

CHEN, Y ;

MORIMOTO, S ;

KITANO, S ;

KOH, E ;

FUKUO, K ;

JIANG, B ;

CHEN, S ;

YASUDA, O ;

HIROTANI, A ;

OGIHARA, T .

ATHEROSCLEROSIS, 1995, 112 (01) :69-76

[3] Role of transactivation of the EGF receptor in signalling by G-protein-coupled receptors [J].

Daub, H ;

Weiss, FU ;

Wallasch, C ;

Ullrich, A .

NATURE, 1996, 379 (6565) :557-560

[4] MAPKS - NEW JNK EXPANDS THE GROUP [J].

DAVIS, RJ .

TRENDS IN BIOCHEMICAL SCIENCES, 1994, 19 (11) :470-473

[5] JNK1 - A PROTEIN-KINASE STIMULATED BY UV-LIGHT AND HA-RAS THAT BINDS AND PHOSPHORYLATES THE C-JUN ACTIVATION DOMAIN [J].

DERIJARD, B ;

HIBI, M ;

WU, IH ;

BARRETT, T ;

SU, B ;

DENG, TL ;

KARIN, M ;

DAVIS, RJ .

CELL, 1994, 76 (06) :1025-1037

[6] Lysophosphatidylcholine stimulates activator protein 1 and the c-Jun N-terminal kinase activity [J].

Fang, XJ ;

Gibson, S ;

Flowers, M ;

Furui, T ;

Bast, RC ;

Mills, GB .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (21) :13683-13689

[7]

FLAVAHAN NA, 1993, AM J PHYSIOL, V264, P722

[8] A MAP KINASE TARGETED BY ENDOTOXIN AND HYPEROSMOLARITY IN MAMMALIAN-CELLS [J].

HAN, J ;

LEE, JD ;

BIBBS, L ;

ULEVITCH, RJ .

SCIENCE, 1994, 265 (5173) :808-811

[9] REGULATION OF PROSTAGLANDIN SYNTHASE-1 AND PROSTAGLANDIN SYNTHASE-2 [J].

HERSCHMAN, HR .

CANCER AND METASTASIS REVIEWS, 1994, 13 (3-4) :241-256

[10] IDENTIFICATION OF AN ONCOPROTEIN-RESPONSIVE AND UV-RESPONSIVE PROTEIN-KINASE THAT BINDS AND POTENTIATES THE C-JUN ACTIVATION DOMAIN [J].

HIBI, M ;

LIN, AN ;

SMEAL, T ;

MINDEN, A ;

KARIN, M .

GENES & DEVELOPMENT, 1993, 7 (11) :2135-2148

← 1 2 3 4 5 →