Activation of the transient receptor potential M2 channel and poly(ADP-ribose) polymerase is involved in oxidative stress-induced cardiomyocyte death
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Bolli R, Mohamed OJ, Patel BS, Aruoma OI, Halliwell B, Lai EK and McCay PB (1989) Marked reduction of free radical generation and contractile dysfunction by antioxidant therapy began at the time of reperfusion: evidence that myocardial ‘stunning’ is a manifestation of reperfusion injury. Circ. Res. 65: 607–622
Colucci WS (1997) Molecular and cellular mechanisms of myocardial failure. Am. J. Cardiol. 80: 15L–25L
Saraste A, Pulkki K, Kallajoki M, Henriksen K, Parvinen M and Voipio-Pulkki L-M (1997) Apoptosis in human acute myocardial infarction. Circulation 95: 320–323
Crow MT, Mani K, Nam Y-J and Kitsis RN (2004) The mitochondrial death pathway and cardiac myocyte apoptosis. Circ. Res. 95: 957–970
Horwitz LD, Fennessey PV, Shikes RH and Kong Y (1994) Marked reduction in myocardial infarct size due to prolonged infusion of an antioxidant during reperfusion. Circulation 89: 1792–1801
Matsumura K, Jeremy RW, Schaper J and Becker LC (1998) Progression of myocardial necrosis during reperfusion of ischemic myocardium. Circulation 97: 795–804
Leist M and Jäättelä M (2001) Four deaths and a funeral: from caspases to alternative mechanisms. Nat. Mol. Cell Biol. 2: 1–10
Green D and Kroemer G (1998) The central executioners of apoptosis: caspases or mitochondria? Trends Cell Biol. 8: 267–271
Petronilli V, Penzo D, Scorrano L, Bernardi P and Di Lisa F (2001) The mitochondrial permeability transition, release of cytochrome c and cell death. J. Biol. Chem. 276: 12030–12034
Newmeyer DD and Ferguson-Miller S (2003) Mitochondria: releasing power for life and unleashing the machineries of death. Cell 112: 481–490
Suleiman M-S, Halestrap AP and Griffiths EJ (2001) Mitochondria: a target for myocardial protection. Pharmacol. Ther. 89: 29–46
Leist M, Single B, Castoldi AE, Kuhnle S and Nicotera P (1997) Intracellular adenosine triphosphate (ATP) concentration: a switch in the decision between apoptosis and necrosis. J. Exp. Med. 185: 1481–1486
Virág L and Szabó C (2002) The therapeutic potential of poly(ADP-ribose) polymerase inhibitors. Pharmacol. Rev. 54: 375–429
Bowes J, McDonald MC, Piper J and Thiemermann C (1999) Inhibitors of poly(ADP-ribose) synthetase protect rat cardiomyocytes against oxidant stress. Cardiovasc. Res. 41: 126–134
Pieper AA, Walles T, Wei G, Clements EE, Verma A, Snyder SH and Zweier JL (2000) Myocardial postischemic injury is reduced by polyADPribose polymerase-1 gene disruption. Mol. Med. 6: 271–282
Buja LM and Entman ML (1998) Modes of myocardial cell injury and cell death in ischemic heart disease. Circulation 98: 1355–1357
Ohno M, Takemura G, Ohno A, Misao J, Hayakawa Y, Minatoguchi S, Fujiwara T and Fujiwara H (1998) Apoptotic myocytes in infarcts area in rabbit hearts may be oncotic myocytes with DNA fragmentation: analysis by immunogold electron microscopy combined with in situ nick end-labeling. Circulation 98: 1422–1430
Dumont EAWJ, Hofstra L, van Heerde WL, van den Eijnde S, Doevendans PAF, DeMuinck E, Daemen MARC, Smits JFM, Frederik P, Wellens HJJ, Daemen MJAP and Reutelingsperger CPM (2000) Cardiomyocyte death induced by myocardial ischemia and reperfusion: measurement with recombinant human annexin-V in a mouse model. Circulation 102: 1564–1568
Van Lookeren Campagne M and Gill R (1996) Ultrastructural morphological changes are not characteristic of apoptotic cell death following focal cerebral ischemia in the rat. Neurosci. Lett. 213: 111–114
Montell C, Birnbaumer L and Flockerzi V (2002) The TRP channels, a remarkably functional family. Cell 108: 595–598
Hara Y, Wakamori M, Ishii M, Maeno E, Nishida M, Yoshida T, Yamada H, Shimizu S, Mori E, Kudoh J, Shimizu N, Kurose H, Okada Y, Imoto K and Mori Y (2002) LTRPC2 Ca2+-permeable channel activated by changes in redox status confers susceptibility to cell death. Mol. Cell 9: 163–173
Wehage E, Eisfeld J, Heiner I, Jüngling E, Zitt C and Lückhoff A (2002) Activation of the cation channel long transient receptor potential channel 2 (LTRPC2) by hydrogen peroxide: a splice variant reveals a mode of activation independent of ADP-ribose. J. Biol. Chem. 277: 23150–23156
McHugh D, Flemming R, Xu S-Z and Perraud A-L (2003) Critical intracellular Ca2+ dependence of transient receptor potential melastatin 2 (TRPM2) cation channel activation. J. Biol. Chem. 278: 11002–11006
Perraud A-L, Fleig A, Dunn CA, Bagley LA, Launay P, Schmitz C, Stokes AJ, Zhu Q, Bessman MJ, Penner R, Kinet J-P and Scharenberg AM (2001) ADP-ribose gating of the calcium-permeable TRRPC2 channel revealed by nudix motif homology. Nature 411: 595–599
Sano Y, Inamura K, Miyake A, Mochizuki S, Yokoi H, Matsushime H and Furuichi K (2001) Immunocyte Ca2+ influx system mediated by LTRPC2. Science 293: 1327–1330
Nieminen A-L, Byrne AM, Brian H and Lemasters JJ (1997) Mitochondrial permeability transition in hepatocytes induced by t-BuOOH: NAD(P)H and reactive oxygen species. Am. J. Physiol. 272: C1286–C1294
Filipovic DM, Meng X and Reeves B (1999) Inhibition of PARP prevents oxidant-induced necrosis but not apoptosis in LLC-PK1 cells. Am. J. Physiol. 277: F428–F436
Ying W, Sevigny MB, Chen Y and Swanson RA (2001) Poly(ADP-ribose) glycohydrolase mediated oxidative and excitotoxic neunal death. Proc. Natl. Acad. Sci. USA 98: 12227–12232
Alvarez-Gonzalez R and Althaus FR (1989) Poly(ADP-ribose) catabolism in mammalian cells exposed to DNA-damaging agents. Mutat. Res. 218: 67–74
D'amours D, Desnoyers S, D'silva I and Poirier GG (1999) Poly(ADP-ribosyl)ation reactions in the regulation of nuclear functions. Biochem. J. 342: 249–268
Küpper JH, de Murcia G and Bürkle A (1990) Inhibition of poly(ADP-ribosylation) by overexpressing the poly(ADP-ribose) polymerase DNA-binding domain in mammalian cells. J. Biol. Chem. 265: 18721–18724
Yang K-T, Pan S-F, Chien C-L, Hsu S-M, Tseng Y-Z, Wang S-M and Wu M-L (2004) Mitochondrial Na+ overload is caused by oxidative stress and leads to activation of the caspase 3-dependent apoptotic machinery. FASEB J. 12: 1442–1444
Chen Z, Alcayaga C, Suárez-Isla BA, O'Rourke B, Tomaselli G and Marbán E (2002) A ‘minimal’ sodium channel construct consisting of ligated S5-P-S6 segments forms a toxin-activatable ionophore. J. Biol. Chem. 277: 24653–24658
Chen W-H, Chu K-C, Wu S-J, Wu J-C, Shui H-A and Wu M-L (1999) Early metabolic inhibition-induced intracellular sodium and calcium increase in rat cerebellar granule cells. J. Physiol. (London) 515: 133–146
Collins TJ, Lipp P, Berridge MJ and Bootman MD (2001) Mitochondrial Ca2+ uptake depends on the spatial and temporal profile of cytosolic Ca2+ signals. J. Biol. Chem. 276: 26411–26420
Matlib MA, Zhou Z, Knight S, Ahmed S, Choi KM, Krause-Bauer J, Philips R, Altschuld R, Katsube Y, Sperelakis N and Bers DM (1998) Oxygen-bridged dinuclear ruthenium amine complex specifically inhibits Ca uptake into mitochondria in vitro and in situ in single cardiac myocytes. J. Biol. Chem. 273: 10223–10231
Gincel D, Zaid H and Shoshan-Barmatz V (2001) Calcium binding and translocation by the voltage-dependent anion channel: a possible regulatory mechanism in mitochondrial function. Biochem. J. 358: 147–155
Jacobson MD, Weil M and Raff MC (1996) Role of Ced-3/ICE-family proteases in staurosporine-induced programmed cell death. J. Cell Biol. 133: 1041–1051
Zhang W, Chu X, Tong Q, Cheung JY, Conrad K, Masker K and Miller BA (2003) A novel TRPM2 isoform inhibits calcium influx and susceptibility to cell death. J. Biol. Chem. 278: 16222–16229
Hill K, McNulty S and Randall AD (2004) Inhibition of TRPM2 channels by the antifungal agents clotrimazole and econazole. Naunyn-Schmiedeberg's Arch. Pharmacol. 370: 227–237
Allen DG, Morris PG, Orchard CH and Pirolo JS (1985) A nuclear magnetic resonance study of metabolism in the ferret heart during hypoxia and inhibition of glycolysis. J. Physiol. (London) 361: 185–204