Poly(ADP-ribose) polymerase - The nuclear target in signal transduction and its role in brain ischemia-reperfusion injury

被引:48
作者
Strosznajder, RP [1 ]
Jesko, H
Zambrzycka, A
机构
[1] Polish Acad Sci, Med Res Ctr, Dept Neurophysiol, Warsaw, Poland
[2] Polish Acad Sci, Med Res Ctr, Dept Cellular Signaling, Warsaw, Poland
关键词
PARP; PARP-1; brain; ischemia; reperfusion; NF-kappa B; p53; neuroprotection;
D O I
10.1385/MN:31:1-3:149
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Poly(ADP-ribose) polymerase (PARP)-l is a DNA nick sensor that transforms ADP-ribose from beta NAD(+) in the form of polymer to over 40 nuclear proteins, particularly to histones, several transcription factors, and PARP itself, modulating their activities and functions. PARP-1 activated by DNA breaks facilitates transcription, replication, and DNA base excision repair. The last studies indicate that PARP-1 is the new nuclear target for fast signals evoked in cell membranes by depolarization and cholinergic and glutaminergic receptors stimulation. Excessive activation of PARP-1 by peroxynitrate-evoked DNA damage during oxidative stress can cause cell death by NAD(+)/ATP depletion after ischemia-reperfusion injury, inflammation, and diabetes mellitus. The PARP-1 through interaction with nuclear factor-kappa beta, p53, and other transcription factors might significantly modulate cell survival and death and a type of death pathway. The pharmacological modulation of PARP-1 might offer a new effective approach for neuroprotection.
引用
收藏
页码:149 / 167
页数:19
相关论文
共 109 条
[1]   Defective induction but normal activation and function of p53 in mouse cells lacking poly-ADP-ribose polymerase [J].
Agarwal, ML ;
Agarwal, A ;
Taylor, WR ;
Wang, ZQ ;
Wagner, EF ;
Stark, GR .
ONCOGENE, 1997, 15 (09) :1035-1041
[2]  
ALTHAUS FR, 1992, J CELL SCI, V102, P663
[3]   PARP-2, a novel mammalian DNA damage-dependent poly(ADP-ribose) polymerase [J].
Amé, JC ;
Rolli, V ;
Schreiber, V ;
Niedergang, C ;
Apiou, F ;
Decker, P ;
Muller, S ;
Hoger, T ;
Murcia, JMD ;
de Murcia, G .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (25) :17860-17868
[4]  
AMSTAD PA, 1992, CANCER RES, V52, P3952
[5]   INHIBITORS AND ACTIVATORS OF ADP-RIBOSYLATION REACTIONS [J].
BANASIK, M ;
UEDA, K .
MOLECULAR AND CELLULAR BIOCHEMISTRY, 1994, 138 (1-2) :185-197
[6]   PATHOLOGICAL IMPLICATIONS OF NITRIC-OXIDE, SUPEROXIDE AND PEROXYNITRITE FORMATION [J].
BECKMAN, JS ;
CROW, JP .
BIOCHEMICAL SOCIETY TRANSACTIONS, 1993, 21 (02) :330-334
[7]  
Bürkle A, 2001, CHEMBIOCHEM, V2, P725, DOI 10.1002/1439-7633(20011001)2:10<725::AID-CBIC725>3.0.CO
[8]  
2-3
[9]  
Chalimoniuk M, 1998, J NEUROSCI RES, V54, P681, DOI 10.1002/(SICI)1097-4547(19981201)54:5<681::AID-JNR13>3.0.CO
[10]  
2-L