Apoptosis-related genes expressed in cardiovascular development and disease: an EST approach

被引:18
作者
Rezvani, M
Barrans, JD
Dai, KS
Liew, CC [1 ]
机构
[1] Univ Toronto, Toronto Gen Hosp, Inst Med Sci, Ctr Cardiovasc Res,Univ Hlth Network, Toronto, ON M5G 1L7, Canada
[2] Univ Toronto, Toronto Gen Hosp, Dept Lab Med & Pathobiol, Ctr Cardiovasc Res,Univ Hlth Network, Toronto, ON M5G 1L7, Canada
基金
英国医学研究理事会;
关键词
apoptosis; developmental biology; gene expression; sequence (DNA/RNA/prot);
D O I
10.1016/S0008-6363(99)00383-1
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Apoptosis (programmmed cell death) is an important process which, in conjunction with cell proliferation, maintains cell number homeostasis, Although apoptosis has been more extensively investigated in other tissues [1,2], only recently has this process been suspected as a significant contributor to both disease and normal development of the cardiovascular system [3-6]. Grasping a comprehension of the underlying genetic mechanisms of apoptosis is especially crucial considering that cardiac myocytes irreversibly exit the cell cycle and thus fail to proliferate during pathological conditions. Despite great strides in understanding the molecular pathways of apoptosis, there still remain numerous questions to be answered. Identifying key genes that are involved in the regulatory process of apoptosis in the cardiovascular system will serve as a basis for creating more effective therapeutic treatments in cardiovascular disease and provide an understanding of how cardiac development is modulated. This review provides a brief summary of recent data implicating genes that may be involved in apoptosis in the cardiovascular system. It also outlines the continued usefulness of large-scale generation of expressed sequence tags (ESTs) to establish expression profiles from the cardiovascular system and as a means of identifying potentially significant apoptotic regulators previously characterized in other tissues but not as yet in the cardiovascular system. (C) 2000 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:621 / 629
页数:9
相关论文
共 82 条
[1]  
Aggarwal S, 1999, J IMMUNOL, V162, P2154
[2]   Involvement of MACH, a novel MORT1/FADD-interacting protease, in Fas/APO-1- and TNF receptor-induced cell death [J].
Boldin, MP ;
Goncharov, TM ;
Goltsev, YV ;
Wallach, D .
CELL, 1996, 85 (06) :803-815
[3]   ADENOVIRUS-E1B 19-KDA AND BCL-2 PROTEINS INTERACT WITH A COMMON SET OF CELLULAR PROTEINS [J].
BOYD, JM ;
MALSTROM, S ;
SUBRAMANIAN, T ;
VENKATESH, LK ;
SCHAEPER, U ;
ELANGOVAN, B ;
DSAEIPPER, C ;
CHINNADURAI, G .
CELL, 1994, 79 (02) :341-351
[4]  
Bruckheimer E M, 1998, Adv Biochem Eng Biotechnol, V62, P75, DOI 10.1007/BFb0102306
[5]   The E1B 19K Bcl-2-binding protein Nip3 is a dimeric mitochondrial protein that activates apoptosis [J].
Chen, G ;
Ray, R ;
Dubik, D ;
Shi, LF ;
Cizeau, J ;
Bleackley, RC ;
Saxena, S ;
Gietz, RD ;
Greenberg, AH .
JOURNAL OF EXPERIMENTAL MEDICINE, 1997, 186 (12) :1975-1983
[6]   Nix and Nip3 form a subfamily of pro-apoptotic mitochondrial proteins [J].
Chen, G ;
Cizeau, J ;
Velde, CV ;
Park, JH ;
Bozek, G ;
Bolton, J ;
Shi, L ;
Dubik, D ;
Greenberg, A .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (01) :7-10
[7]   STRETCH-INDUCED PROGRAMMED MYOCYTE CELL-DEATH [J].
CHENG, W ;
LI, BS ;
KAJSTURA, J ;
LI, P ;
WOLIN, MS ;
SONNENBLICK, EH ;
HINTZE, TH ;
OLIVETTI, G ;
ANVERSA, P .
JOURNAL OF CLINICAL INVESTIGATION, 1995, 96 (05) :2247-2259
[8]   Stage-specific apoptosis, developmental delay, and embryonic lethality in mice homozygous for a targeted disruption in the murine Bloom's syndrome gene [J].
Chester, N ;
Kuo, F ;
Kozak, C ;
O'Hara, CD ;
Leder, P .
GENES & DEVELOPMENT, 1998, 12 (21) :3382-3393
[9]   FADD, A NOVEL DEATH DOMAIN-CONTAINING PROTEIN, INTERACTS WITH THE DEATH DOMAIN OF FAS AND INITIATES APOPTOSIS [J].
CHINNAIYAN, AM ;
OROURKE, K ;
TEWARI, M ;
DIXIT, VM .
CELL, 1995, 81 (04) :505-512
[10]  
Chinnaiyan AM, 1996, J BIOL CHEM, V271, P4961