Apoptotic cell death and caspase 3 (CPP32) activation induced by calcium ionophore at low concentrations and their prevention by nerve growth factor in PC12 cells

被引:43
作者
Takadera, T
Ohyashiki, T
机构
[1] Department of Clinical Chemistry, Faculty of Pharmaceutical Sciences, Hokuriku University, Kanazawa
[2] Department of Clinical Chemistry, Faculty of Pharmaceutical Sciences, Hokuriku University, Kanazawa
来源
EUROPEAN JOURNAL OF BIOCHEMISTRY | 1997年 / 249卷 / 01期
关键词
calcium; apoptosis; nerve-growth factor; caspase-3 (CPP32); PC12; cells;
D O I
10.1111/j.1432-1033.1997.00008.x
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
A23187 (a calcium ionophore) at law concentration (0.1 mu M) induced apoptotic cell death (chromatin condensation and DNA fragmentation) accompanied by the activation of caspase-3 (CPP32), a member of the interleukin-1 beta-converting enzyme protease. On the other hand, A23187 at high concentration (2 mu M) induced neurotic cell death not accompanied by the activation of CPP32, Nerve growth factor inhibited the cell death and CPP32 activation induced by 0.1 mu M A23187, but not the fell death induced by 2 mu M A23187, Acylaspartyl-glutamyl-valyl-aspartyl-aldehyde, an inhibitor of CPP32. reduced the cell death induced by 0.1 mu M A23187. These results suggest that calcium-ion-induced apoptotic cell death was mediated by CPP32 activation in PC12 cells.
引用
收藏
页码:8 / 12
页数:5
相关论文
共 29 条
[1]   APOPTOSIS AND NECROSIS - 2 DISTINCT EVENTS INDUCED, RESPECTIVELY, BY MILD AND INTENSE INSULTS WITH N-METHYL-D-ASPARTATE OR NITRIC-OXIDE SUPEROXIDE IN CORTICAL CELL-CULTURES [J].
BONFOCO, E ;
KRAINC, D ;
ANKARCRONA, M ;
NICOTERA, P ;
LIPTON, SA .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (16) :7162-7166
[2]   Mitogen-activated protein kinase-independent pathways mediate the effects of nerve growth factor and cAMP on neuronal survival [J].
Creedon, DJ ;
Johnson, EM ;
Lawrence, JC .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1996, 271 (34) :20713-20718
[3]   GLUTAMATE-INDUCED NEURONAL DEATH IS NOT A PROGRAMMED CELL-DEATH IN CEREBELLAR CULTURE [J].
DESSI, F ;
CHARRIAUTMARLANGUE, C ;
KHRESTCHATISKY, M ;
BENARI, Y .
JOURNAL OF NEUROCHEMISTRY, 1993, 60 (05) :1953-1955
[4]   Sequential activation of ICE-like and CPP32-like proteases during Fas-mediated apoptosis [J].
Enari, M ;
Talanian, RV ;
Wong, WW ;
Nagata, S .
NATURE, 1996, 380 (6576) :723-726
[5]   A BIOCHEMICAL FUNCTION FOR RAS - AT LAST [J].
HALL, A .
SCIENCE, 1994, 264 (5164) :1413-1414
[6]  
HARTIKKA J, 1988, J NEUROSCI, V8, P2967
[7]   BCL-2 IS AN INNER MITOCHONDRIAL-MEMBRANE PROTEIN THAT BLOCKS PROGRAMMED CELL-DEATH [J].
HOCKENBERY, D ;
NUNEZ, G ;
MILLIMAN, C ;
SCHREIBER, RD ;
KORSMEYER, SJ .
NATURE, 1990, 348 (6299) :334-336
[8]   MOLECULAR MECHANISMS OF DEVELOPMENTAL NEURONAL DEATH [J].
JOHNSON, EM ;
DECKWERTH, TL .
ANNUAL REVIEW OF NEUROSCIENCE, 1993, 16 :31-46
[9]   NEURONAL DEATH, CYTOPLASMIC CALCIUM AND INTERNUCLEOSOMAL DNA-FRAGMENTATION - EVIDENCE FOR DNA-FRAGMENTS BEING RELEASED FROM CELLS [J].
JOSEPH, R ;
LI, W ;
HAN, E .
MOLECULAR BRAIN RESEARCH, 1993, 17 (1-2) :70-76
[10]   Decreased apoptosis in the brain and premature lethality in CPP32-deficient mice [J].
Kuida, K ;
Zheng, TS ;
Na, SQ ;
Kuan, CY ;
Yang, D ;
Karasuyama, H ;
Rakic, P ;
Flavell, RA .
NATURE, 1996, 384 (6607) :368-372