Mining for survival genes

被引：3
作者：
Dawson, V. L.
Dawson, T. M.
机构：
[1] Johns Hopkins Univ, Sch Med, Inst Cell Engn, Dept Neurol, Baltimore, MD 21205 USA
[2] Johns Hopkins Univ, Sch Med, Dept Neurol, Inst Cell Engn, Baltimore, MD 21205 USA
[3] Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA
[4] Johns Hopkins Univ, Sch Med, Dept Physiol, Baltimore, MD 21205 USA
来源：
BIOCHEMICAL SOCIETY TRANSACTIONS | 2006年 / 34卷
关键词：
brain; excitotoxicity; ischaemia; preconditioning; stroke;
D O I：
10.1042/BST0341307
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：
many stressful, but not lethal, stimuli activate endogenous protective mechanisms that significantly decrease the degree of injury to subsequent injurious stimuli. This protective mechanism is termed preconditioning and tolerance. it occurs across organ systems including the brain and nervous system. Preconditioning has been investigated in cell and animal models and recently been shown to potentially occur in human brain. Learning more about these powerful endogenous neuroprotective mechanisms could help identify new approaches to treat patients with stroke and other central nervous system disorders or injury. Cell and animal models are helping us to better understand the network response of gene and protein expression that activates the neuroprotective response.
引用
收藏
页码：1307 / 1309
页数：3
相关论文
共 35 条
[1]  
Aizenman E, 2000, J PHARMACOL EXP THER, V295, P572
[2]   Bilateral ischemic tolerance of rat hippocampus induced by prior unilateral transient focal ischemia: Relationship to c-fos mRNA expression [J].
Belayev, L ;
Ginsberg, MD ;
Alonso, OF ;
Singer, JT ;
Zhao, WZ ;
Busto, R .
NEUROREPORT, 1996, 8 (01) :55-59
[3]   Nitric oxide is involved in anoxic preconditioning neuroprotection in rat hippocampal slices [J].
Centeno, JM ;
Orti, MA ;
Salom, JB ;
Sick, TJ ;
Pérez-Pinzón, MA .
BRAIN RESEARCH, 1999, 836 (1-2) :62-69
[4]   TRANSIENT HYPERTHERMIA PROTECTS AGAINST SUBSEQUENT FOREBRAIN ISCHEMIC CELL-DAMAGE IN THE RAT [J].
CHOPP, M ;
CHEN, H ;
HO, KL ;
DERESKI, MO ;
BROWN, E ;
HETZEL, FW ;
WELCH, KMA .
NEUROLOGY, 1989, 39 (10) :1396-1398
[5]   Benign focal ischemic preconditioning induces neuronal Hsp70 and prolonged astrogliosis with expression of Hsp27 [J].
Currie, RW ;
Ellison, JA ;
White, RF ;
Feuerstein, GZ ;
Wang, XK ;
Barone, FC .
BRAIN RESEARCH, 2000, 863 (1-2) :169-181
[6]   Nitric oxide mediates cerebral ischemic tolerance in a neonatal rat model of hypoxic preconditioning [J].
Gidday, JM ;
Shah, AR ;
Maceren, RG ;
Wang, QO ;
Pelligrino, DA ;
Holtzman, DM ;
Park, TS .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1999, 19 (03) :331-340
[7]   Requirement for nitric oxide activation of p21ras/extracellular regulated kinase in neuronal ischemic preconditioning [J].
Gonzalez-Zulueta, M ;
Feldman, AB ;
Klesse, LJ ;
Kalb, RG ;
Dillman, JF ;
Parada, LF ;
Dawson, TM ;
Dawson, VL .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (01) :436-441
[8]  
Grabb MC, 1999, J NEUROSCI, V19, P1657
[9]   NORMAL ACTIVATION OF P70 S6 KINASE BY INSULIN IN CELLS OVEREXPRESSING DOMINANT-NEGATIVE 85KD SUBUNIT OF PHOSPHOINOSITIDE 3-KINASE [J].
HARA, K ;
YONEZAWA, K ;
SAKAUE, H ;
KOTANI, K ;
KOTANI, K ;
KOJIMA, A ;
WATERFIELD, MD ;
KASUGA, M .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1995, 208 (02) :735-741
[10]   ESSENTIAL ROLE OF ADENOSINE, ADENOSINE-A1-RECEPTORS, AND ATP-SENSITIVE K+ CHANNELS IN CEREBRAL ISCHEMIC PRECONDITIONING [J].
HEURTEAUX, C ;
LAURITZEN, I ;
WIDMANN, C ;
LAZDUNSKI, M .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (10) :4666-4670
1234