The mitochondria are recognition organelles of cell stress

被引:9
作者
Lai, YK
Lee, WC
Hu, CH
Hammond, GL
机构
[1] YALE UNIV, SCH MED, DEPT SURG, NEW HAVEN, CT 06520 USA
[2] NATL TSING HUA UNIV, DEPT LIFE SCI, HSINCHU 30043, TAIWAN
[3] PIG RES INST, DEPT COMPARAT MED, CHUNAN 35099, SOUTH KOREA
关键词
D O I
10.1006/jsre.1996.0179
中图分类号
R61 [外科手术学];
学科分类号
摘要
The cellular response to stress includes synthesis of specific stress proteins in the presence of a generalized suppression of protein synthesis. The response occurs in intact animals, individually stressed organs of intact animals, donor organs upon removal, regardless of preservation methods, and cells in culture. The molecular biology of stress protein induction is not understood. While stress proteins are beneficial, overall suppression of protein synthesis, if prolonged, is harmful. Since altered energy metabolism is integral to stress induction, we examined the mitochondria to determine if they could provide a possible molecular mechanism for initiating the response. Rat myoblasts were incubated at varying temperatures for up to 120 min in [S-35]methionine. Proteins were separated electrophoretically and newly synthesized proteins visualized autoradiographically. Isolated mitochondria from resting rat myoblasts were then stressed, label incorporation determined, and newly synthesized protein was visualized. Stress sharply suppressed protein synthesis in mitochondria but autoradiograms of stressed mitochondria showed that a single stress protein of 18 kDa was synthesized. Mitochondria independently respond to stress and synthesize a stress protein from their own DNA. This protein may provide an intermediary pathway that links stressful conditions in the environment to the overall response observed in the cell. (C) 1996 Academic Press, Inc.
引用
收藏
页码:90 / 94
页数:5
相关论文
共 29 条
[1]  
ALBERTS B, 1989, MOL BIOL CELL, P88
[2]   ABNORMAL PROTEINS SERVE AS EUKARYOTIC STRESS SIGNALS AND TRIGGER THE ACTIVATION OF HEAT-SHOCK GENES [J].
ANANTHAN, J ;
GOLDBERG, AL ;
VOELLMY, R .
SCIENCE, 1986, 232 (4749) :522-524
[3]  
CHENG MY, 1990, NATURE, V348, P55
[4]  
GEORGOPOULOS C, 1989, STRESS INDUCED PROTE, V96, P37
[5]   HEAT-SHOCK REGULATORY GENE HTPR INFLUENCES RATES OF PROTEIN-DEGRADATION AND EXPRESSION OF THE ION GENE IN ESCHERICHIA-COLI [J].
GOFF, SA ;
CASSON, LP ;
GOLDBERG, AL .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-BIOLOGICAL SCIENCES, 1984, 81 (21) :6647-6651
[6]   PRELIMINARY CHARACTERIZATION OF MOLECULES THAT INCREASE CELL FREE TRANSLATIONAL ACTIVITY OF CARDIAC CYTOPLASMIC RNA [J].
HAMMOND, GL ;
LAI, YK ;
MARKERT, CL .
EUROPEAN HEART JOURNAL, 1984, 5 :225-229
[7]   DIVERSE FORMS OF STRESS LEAD TO NEW PATTERNS OF GENE-EXPRESSION THROUGH A COMMON AND ESSENTIAL METABOLIC PATHWAY [J].
HAMMOND, GL ;
LAI, YK ;
MARKERT, CL .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-BIOLOGICAL SCIENCES, 1982, 79 (11) :3485-3488
[8]  
HAMMOND GL, 1996, GLENNS THORACIC CARD, V11, P1561
[9]  
HAMMOND GL, 1987, STRESSED HEART, P21
[10]  
HAVRE PA, 1988, AM J PHYSIOL, V255, pH1024, DOI 10.1152/ajpheart.1988.255.5.H1024