Differential role of glutaredoxin and thioredoxin in metabolic oxidative stress-induced activation of apoptosis signal-regulating kinase 1

被引:146
作者
Song, JJ
Lee, YJ [1 ]
机构
[1] Univ Pittsburgh, Hillman Canc Ctr, Dept Surg, Pittsburgh, PA 15213 USA
[2] Univ Pittsburgh, Hillman Canc Ctr, Inst Canc, Pittsburgh, PA 15213 USA
关键词
apoptosis signal-regulating kinase 1; glucose deprivation; glutaredoxin; glutathione; metabolic oxidative stress; thioredoxin;
D O I
10.1042/BJ20030275
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
Redox-sensing molecules such as thioredoxin (TRX) and gluta-redoxin (GRX) bind to apoptosis signal-regulating kinase 1 (ASK1) and suppress its activation. Glucose deprivation disrupted the interaction between TRX/GRX and ASK1 and subsequently activated the ASK 1-stress-activated protein kinase/extracellular-signal-regulated kinase kinase-c-Jun N-terminal kinase 1 (JNK1) signal-transduction pathway. L-Buthionine-(S,R)sulphoximine, which decreases intracellular glutathione content, enhanced glucose deprivation-induced activation of JNK1 by promoting the dissociation of TRX, but not GRX, from ASK1. Treatment of cells with exogenous glutathione disulphide ester resulted in the dissociation of GRX, but not TRX, from ASK1 and the subsequent activation of JNK1. Nonetheless, overexpression of calatase, an H2O2 scavenger, inhibited JNK1 activation and cytotoxicity as well as the dissociation of TRX and GRX from ASK1 during combined glucose deprivation and L-buthionine(S,R)-sulphoximine treatment. Taken together, glucose deprivation-induced metabolic oxidative stress may activate ASK1 through two different pathways: glutathione-dependent GRX-ASK1 and glutathione-independent TRX-ASK1 pathways.
引用
收藏
页码:845 / 853
页数:9
相关论文
共 41 条
  • [1] Metabolic oxidative stress activates signal transduction and gene expression during glucose deprivation in human tumor cells
    Blackburn, RV
    Spitz, DR
    Liu, X
    Galoforo, SS
    Sim, JE
    Ridnour, LA
    Chen, JC
    Davis, BH
    Corry, PM
    Lee, YJ
    [J]. FREE RADICAL BIOLOGY AND MEDICINE, 1999, 26 (3-4) : 419 - 430
  • [2] Cysteine-to-alanine replacements in the Escherichia coli SoxR protein and the role of the [2Fe-2S] centers in transcriptional activation
    Bradley, TM
    Hidalgo, E
    Leautaud, V
    Ding, H
    Demple, B
    [J]. NUCLEIC ACIDS RESEARCH, 1997, 25 (08) : 1469 - 1475
  • [3] Triggering and modulation of apoptosis by oxidative stress
    Chandra, J
    Samali, A
    Orrenius, S
    [J]. FREE RADICAL BIOLOGY AND MEDICINE, 2000, 29 (3-4) : 323 - 333
  • [4] Dissecting Fas signaling with an altered-specificity death-domain mutant: Requirement of FADD binding for apoptosis but not Jun N-terminal kinase activation
    Chang, HY
    Yang, XL
    Baltimore, D
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (04) : 1252 - 1256
  • [5] Activation of apoptosis signal regulating kinase 1 (ASK1) by the adapter protein Daxx
    Chang, HY
    Nishitoh, H
    Yang, XL
    Ichijo, H
    Baltimore, D
    [J]. SCIENCE, 1998, 281 (5384) : 1860 - 1863
  • [6] Acute cadmium exposure inactivates thioltransferase (glutaredoxin), inhibits intracellular reduction of protein-glutathionyl-mixed disulfides, and initiates apoptosis
    Chrestensen, CA
    Starke, DW
    Mieyal, JJ
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (34) : 26556 - 26565
  • [7] H2O2 sensing through oxidation of the Yap1 transcription factor
    Delaunay, A
    Isnard, AD
    Toledano, MB
    [J]. EMBO JOURNAL, 2000, 19 (19) : 5157 - 5166
  • [8] In vivo kinetics of a redox-regulated transcriptional switch
    Ding, HG
    Demple, B
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (16) : 8445 - 8449
  • [9] Hydrogen peroxide removal and glutathione mixed disulfide formation during metabolic inhibition in mesencephalic cultures
    Ehrhart, J
    Zeevalk, GD
    [J]. JOURNAL OF NEUROCHEMISTRY, 2001, 77 (06) : 1496 - 1507
  • [10] GRIFFITH OW, 1982, J BIOL CHEM, V257, P13704