NERVE GROWTH-FACTOR AND EPIDERMAL GROWTH-FACTOR RESCUE PC12 CELLS FROM PROGRAMMED CELL-DEATH INDUCED BY ETOPOSIDE - DISTINCT MODES OF PROTECTION AGAINST CELL-DEATH BY GROWTH-FACTORS AND A PROTEIN-SYNTHESIS INHIBITOR

被引：27

作者：

NAKAJIMA, M ^{[1
]}

KASHIWAGI, K ^{[1
]}

OHTA, J ^{[1
]}

FURUKAWA, S ^{[1
]}

HAYASHI, K ^{[1
]}

KAWASHIMA, T ^{[1
]}

HAYASHI, Y ^{[1
]}

机构：

[1] GIFU PHARMACEUT UNIV,DEPT MOLEC BIOL,GIFU 502,JAPAN

来源：

NEUROSCIENCE LETTERS | 1994年 / 176卷 / 02期

关键词：

PC12; CELL; PROGRAMMED CELL DEATH; ETOPOSIDE; NERVE GROWTH FACTOR; EPIDERMAL GROWTH FACTOR; CYCLOHEXIMIDE; ACTINOMYCIN D;

D O I：

10.1016/0304-3940(94)90072-8

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

A rat pheochromocytoma cell line (PC12 cells) died within 24 h in the presence of etoposide (1-40 mu g/ml), an inhibitor of topoisomerase II. This cytotoxic effect was prevented by either nerve growth (NGF) or epidermal growth factor (EGF). Cycloheximide and actinomycin D also suppressed the cell death as well. Furthermore, a difference among protective modes against etoposide-induced death by growth factors and a protein-synthesis inhibitor was observed: the protective effect of either NGF or EGF remained rather constant as a function of incubation time with etoposide whereas that of cycloheximide declined. These results indicate that etoposide induces programmed death in PC12 cells and that prevention of the programmed cell death by both NGF and EGF is mainly due to inactivation of molecules involved in the death processes rather than suppression of specific protein and/or mRNA synthesis.

引用

页码：161 / 164

页数：4

共 12 条

[1] AURINTRICARBOXYLIC ACID RESCUES PC12 CELLS AND SYMPATHETIC NEURONS FROM CELL-DEATH CAUSED BY NERVE GROWTH-FACTOR DEPRIVATION - CORRELATION WITH SUPPRESSION OF ENDONUCLEASE ACTIVITY [J].