Mitochondrial dysfunction and oxidative stress as determinants of cell death/survival in stroke

Annals of the New York Academy of Sciences

Volumn 1042, Issue , 2005, Pages 203-209

  Chan, Pak H ^a,b  

^a STANFORD UNIVERSITY SCHOOL OF MEDICINE   (United States)

^b STANFORD UNIVERSITY   (United States)

Author keywords

Akt PKB; Apoptosis; Bad; Cerebral ischemia; Mitochondrion; Oxidative stress; PI3 kinase

Indexed keywords

ADENOSINE TRIPHOSPHATE; CASPASE 3; CASPASE 9; CYTOCHROME C; DNA FRAGMENT; PHOSPHATIDYLINOSITOL 3 KINASE; PROTEIN 14 3 3; PROTEIN BAD; PROTEIN BCL XL; PROTEIN KINASE B; REACTIVE OXYGEN METABOLITE; SECOND MITOCHONDRIAL ACTIVATOR OF CASPASE; SUPEROXIDE DISMUTASE;

APOPTOSIS; BRAIN INJURY; BRAIN ISCHEMIA; CELL DEATH; CELL SURVIVAL; CONFERENCE PAPER; DISORDERS OF MITOCHONDRIAL FUNCTIONS; ENZYME ACTIVATION; GENE OVEREXPRESSION; HUMAN; MOUSE; NERVE DEGENERATION; NONHUMAN; OXIDATION REDUCTION STATE; OXIDATIVE PHOSPHORYLATION; OXIDATIVE STRESS; PROTEIN BINDING; RESPIRATORY CHAIN; SIGNAL TRANSDUCTION; STROKE;

EID: 22044455324     PISSN: 00778923     EISSN: None     Source Type: Book Series    
DOI: 10.1196/annals.1338.022     Document Type: Conference Paper

References (31)

1. BOYER, P.D. et al. 1977. Oxidative phosphorylation and photophosphorylation. Ann. Rev. Biochem. 46: 955-026.
2. FUJIMURA, M. et al. 1998. Cytosolic redistribution of cytochrome c after transient focal cerebral ischemia in rats. J. Cereb. Blood Flow Metab. 18: 1239-1247.
3. SUGAWARA, T. et al. 1999. Mitochondrial release of cytochrome c corresponds to the selective vulnerability of hippocampal CA1 neurons in rats after transient global cerebral ischemia. J. Neurosci. 19: 1-6.
4. FUJIMURA, M. et al. 2000. The cytosolic antioxidant copper/zinc- superoxide dismutase prevents the early release of mitochondrial cytochrome c in ischemic brain after transient focal cerebral ischemia in mice. J. Neurosci. 20: 2817-2824.
5. GREEN, D.R. & J.C. REED. 1998. Mitochondria and apoptosis. Science 281: 1309-1312.
6. KUIDA, K. et al. 1998. Reduced apoptosis and cytochrome c-mediated caspase activation in mice lacking caspase 9. Cell 94: 325-337.
7. LI, P. et al. 1997. Cytochrome c and dATP-dependent formation of Apaf-1/caspase-9 complex initiates an apoptotic protease cascade. Cell 91: 479-489.
8. YOSHIDA, H. et al. 1998. Apaf1 is required for mitochondrial pathways of apoptosis and brain development. Cell 94: 739-750.
9. SLEE, E.A. et al. 1999. Ordering the cytochrome c-initiated caspase cascade: hierarchical activation of caspases-2, -3, -6, -7, -8, and -10 in a caspase-9-dependent manner. J. Cell Biol. 144:281-292.
10. SUGAWARA, T. et al. 2002. Overexpression of copper/zinc superoxide dismutase in transgenic rats protects vulnerable neurons against ischémic damage by blocking the mitochondrial pathway of caspase activation. J. Neurosci. 22: 209-217.
11. DEVERAUX, Q.L. & J.C. REED. 1999. IAP family proteins-suppressors of apoptosis. Genes Dev. 13: 239-252.
12. MILLER, L.K. 1999. An exegesis of IAPs: salvation and surprises from BIR motifs. Trends Cell Biol. 9: 323-328.
13. CHAI, J. et al. 2000. Structural and biochemical basis of apoptotic activation by Smac/ DIABLO. Nature 406: 855-862.
14. NOSHITA, N. et al. 2001. Manganese superoxide dismutase affects cytochrome c release and caspase-9 activation after transient focal cerebral ischemia in mice. J. Cereb. Blood Flow Metab. 21: 557-567.
15. KIM, G.W. et al. 2002. Manganese superoxide dismutase deficiency exacerbates cerebral infarction after focal cerebral ischemia/reperfusion in mice. Implications for the production and role of superoxide radicals. Stroke 33: 809-815.
16. SUGAWARA, T. et al. 2002. Overexpression of SOD1 protects vulnerable motor neurons after spinal cord injury by attenuating mitochondrial cytochrome c release. FASEB J. express article 10.1096/fj.02-0251fje; summary. FASEB J. 16: 1997-1999.
17. FUJIMURA, M. et al. 1999. Copper-zinc superoxide dismutase prevents the early decrease of apurinic/apyrimidinic endonuclease and subsequent DNA fragmentation after transient focal cerebral ischemia in mice. Stroke 30: 2408-2415.
18. SAITO, A. et al. 2004. Oxidative stress is associated with XIAP and Smac/DIABLO signaling pathways in mouse brains after transient focal cerebral ischemia. Stroke 35: 1443-1448.
19. YUAN, J. & B.A. YANKNER. 2000. Apoptosis in the nervous system. Nature 407: 802-809.
20. SHI, Y. 2001. A structural view of mitochondria-mediated apoptosis. Nat. Struct. Biol. 8: 394-401.
21. MARTINOU, J.-C. et al. 1994. Overexpression of BCL-2 in transgenic mice protects neurons from naturally occurring cell death and experimental ischemia. Neuron 13: 1017-1030.
22. YANG, E. et al. 1995. Bad, a heterodimeric partner for Bel-XL and Bcl-2, displaces Bax and promotes cell death. Cell 80: 285-291.
23. ZHA, J. et al. 1996. Serine phosphorylation of death agonist BAD in response to survival factor results in binding to 14-3-3 not BCL-X(L). Cell 87: 619-628.
24. SAITO, A. et al. 2003. Overexpression of copper/zinc superoxide dismutase in transgenic mice protects against neuronal cell death after transient focal ischemia by blocking activation of the Bad cell death signaling pathway. J. Neurosci. 23: 1710-1718.
25. CARDONE, M.H. et al. 1998. Regulation of cell death protease caspase-9 by phosphorylation. Science 282: 1318-1321.
26. BRUNET, A. et al. 1999. Akt promotes cell survival by phosphorylating and inhibiting a Forkhead transcription factor. Cell 96: 857-868.
27. BOULTON, T.G. et al. 1991. ERKs: a family of protein-serine/threonine kinases that are activated and tyrosine phosphorylated in response to insulin and NGF. Cell 65: 663-675.
28. ZHU, Y. et al. 2002. Transforming growth factor-β1 increases Bad phosphorylation and protects neurons against damage. J. Neurosci. 22: 3898-3909.
29. NOSHITA, N. et al. 2002. Copper/zinc superoxide dismutase attenuates neuronal cell death by preventing extracellular signal-regulated kinase activation after transient focal cerebral ischemia in mice. J. Neurosci. 22: 7923-7930.
30. 155. Biochem. J. 349: 547-557.
31. KIMURA, S. et al. 1998. cAMP-dependent long-term potentiation of nitric oxide release from cerebellar parallel fibers in rats. J. Neurosci. 18: 8551-8558.