Development-dependent disappearance of caspase-3 in skeletal muscle is post-transcriptionally regulated

被引:30
作者
Ruest, LB
Khalyfa, A
Wang, E
机构
[1] Univ Louisville, Dept Biochem & Mol Biol, Sch Med, Louisville, KY 40202 USA
[2] Sir Mortimer B Davis Jewish Hosp, Lady Davis Inst Med Res, Bloomfield Ctr Res Aging, Montreal, PQ, Canada
[3] McGill Univ, Dept Med, Montreal, PQ, Canada
关键词
skeletal muscle; development; caspase-3; apoptosis; mRNA; protein; post-transcriptional regulation; muscle regeneration;
D O I
10.1002/jcb.10211
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
Caspase-3, a major player in apoptosis, engages apoptosis-activated cells into an irreversible pathway leading to cell death. In this article, we report that caspase-3 protein is absent from rat and mouse adult skeletal muscles, despite the abundant presence of its mRNA. During skeletal muscle development, caspase-3 protein is present in neonatal animals, but its expression gradually decreases, and disappears completely by I month of age, when there is still abundant caspase-3 mRNA. This discordance between caspase-3 message and protein expression is unique to skeletal muscle, as in all other analyzed tissues the protein presence correlates with the presence of the mRNA. The only circumstance in which caspase-3 protein appears in adults is in regenerating muscles; once regeneration is complete, however, it again becomes undetectable in repaired muscles. We conclude that caspase-3 protein in skeletal muscle is uniquely regulated at the post-transcriptional level, unseen in other tissues such as brain, heart, lung, kidney, thymus, spleen, liver, or testis. The post-transcriptional regulation of caspase-3 might serve as a fail-safe mechanism to avoid accidental cell death. (C) 2002 Wiley-Liss, Inc.
引用
收藏
页码:21 / 28
页数:8
相关论文
共 37 条
[1]   Biochemical pathways of caspase activation during apoptosis [J].
Budihardjo, I ;
Oliver, H ;
Lutter, M ;
Luo, X ;
Wang, XD .
ANNUAL REVIEW OF CELL AND DEVELOPMENTAL BIOLOGY, 1999, 15 :269-290
[2]   Human skeletal muscle cytosols are refractory to cytochrome c-dependent activation of type-II caspases and lack APAF-1 [J].
Burgess, DH ;
Svensson, M ;
Dandrea, T ;
Grönlund, K ;
Hammarquist, F ;
Orrenius, S ;
Cotgreave, IA .
CELL DEATH AND DIFFERENTIATION, 1999, 6 (03) :256-261
[3]   The lethal mutation of the mouse wasted (wst) is a deletion that abolishes expression of a tissue-specific isoform of translation elongation factor 1α, encoded by the Eefla2 gene [J].
Chambers, DM ;
Peters, J ;
Abbott, CM .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (08) :4463-4468
[4]   Apoptosis and atrophy in rat slow skeletal muscles in chronic heart failure [J].
Dalla Libera, L ;
Zennaro, R ;
Sandri, M ;
Ambrosio, GB ;
Vescovo, G .
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, 1999, 277 (05) :C982-C986
[5]  
FERNANDESALNEMRI T, 1994, J BIOL CHEM, V269, P30761
[6]   Caspases:: key players in programmed cell death [J].
Grütter, MG .
CURRENT OPINION IN STRUCTURAL BIOLOGY, 2000, 10 (06) :649-655
[7]   Apoptosis: Molecular regulation of cell death [J].
Hale, AJ ;
Smith, CA ;
Sutherland, LC ;
Stoneman, VEA ;
Longthorne, VL ;
Culhane, AC ;
Williams, GT .
EUROPEAN JOURNAL OF BIOCHEMISTRY, 1996, 236 (01) :1-26
[8]  
Juan TSC, 1996, ONCOGENE, V13, P749
[9]   APOPTOSIS - BASIC BIOLOGICAL PHENOMENON WITH WIDE-RANGING IMPLICATIONS IN TISSUE KINETICS [J].
KERR, JFR ;
WYLLIE, AH ;
CURRIE, AR .
BRITISH JOURNAL OF CANCER, 1972, 26 (04) :239-+
[10]  
Khalyfa A, 1999, DEV DYNAM, V216, P267, DOI 10.1002/(SICI)1097-0177(199911)216:3<267::AID-DVDY5>3.3.CO