ROLE OF PROTEIN-KINASE-C IN THE INHIBITION BY FIBROBLAST GROWTH-FACTOR OF APOPTOSIS IN SERUM-DEPLETED ENDOTHELIAL-CELLS

被引:121
作者
ARAKI, S
SIMADA, Y
KAJI, K
HAYASHI, H
机构
[1] NAGOYA UNIV, SCH SCI,SUGASHIMA MARINE BIOL LAB, 429-63 SUGASHIMA CHO,CHIKUSA KU, TOBA, MIE 517, JAPAN
[2] NAGOYA UNIV, DEPT MOLEC BIOL, CHIKUSA KU, TOBA, MIE 517, JAPAN
[3] NATL INST RADIOL SCI, CHIBA 260, JAPAN
[4] TOKYO METROPOLITAN GERIATR HOSP & INST GERONTOL, ITABASHI KU, TOKYO 173, JAPAN
关键词
D O I
10.1016/0006-291X(90)91557-9
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
Apoptosis in vascular endothelial cells is suppressed by fibroblast growth factor (FGF)1. In order to investigate the signal transduction system that regulates endothelial apoptosis, we studied the effects of several mitogenic factors. Apoptosis occurred in human vascular endothelial cells under serum-free conditions, and FGF inhibited apoptosis without a requirement of any cooperative factors, as distinct from the mitogenic response. Other mitogenic agents, such as epidermal growth factor, transferrin, transforming growth factor beta, and interleukin 1 etc., with the exception of dexamethasone, had no such inhibitory effects. The effect of FGF was mimicked by a phorbol ester and was prevented by an inhibitor of protein kinase C. The results suggest that the FGF and protein kinase C are important in endothelial apoptosis. © 1990.
引用
收藏
页码:1081 / 1085
页数:5
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