[an error occurred while processing this directive]
en

A new form of cell death: Parthanatos

Expand
  • Laboratory of Development Biology, College of Life Science, Northeast Forestry University, Harbin 150040, China

Received date: 2009-11-26

  Revised date: 2010-01-20

  Online published: 2010-09-20

Abstract

Parthanatos is a form of cell death, which often occurs in many diseases such as stroke, Parkinson’s disease, heart attack, diabetes, and ischemia reperfusion injury. In a cell, the activation of PARP-1 caused by excitotoxicity leads to Parthanatos, which is also known as PARP-1-dependent cell death. There are multiple cell signaling pathways involved in the process of Parthanatos, which have not been fully understood. The main focus of this article is underlying molecular mechanisms of Parthanatos.

Key words: Parthanatos; PARP-1; PAR; AIF; cell death

Cite this article

WANG Lian-Bang, ZHANG Li-Yang, CHAN Chun-Hua . A new form of cell death: Parthanatos[J]. Hereditas(Beijing), 2010 , 32(9) : 881 -885 . DOI: 10.3724/SP.J.1005.2010.00881

References

[1] Harraz MM, Dawson TM, Dawson VL. Advances in neu-ronal cell death 2007. Stroke, 2008, 39(2): 286-288. [2] Yu SW, Wang H, Poitras MF, Coombs C, Bowers WJ, Federoff HJ, Poirier GG, Dawson TM, Dawson VL. Me-diation of poly(ADP-ribose) polymerase-1-dependent cell death by apoptosis-inducing factor. Science, 2002, 297(5579): 259-263. [3] Andrabi SA, Kim NS, Yu SW, Wang H, Koh DW, Sasaki M, Klaus JA, Otsuka T, Zhang Z, Koehler RC, Hurn PD, Poirier GG, Dawson VL, Dawson TM. Poly(ADP-ribose) (PAR) polymer is a death signal. Proc Natl Acad Sci USA, 2006, 103(48): 18308–18313. [4] Yu SW, Andrabi SA, Wang H, Kim NS, Poirier GG, Dawson TM, Dawson VL. Apoptosis-inducing factor medi-ates poly(ADP-ribose) (PAR) polymer-induced cell death. Proc Natl Acad Sci USA, 2006, 103(48): 18314–18319. [5] David KK, Andrabi SA, Dawson TM, Dawson VL. Par-thanatos, a messenger of death. Front Biosci, 2009, 14: 1116–1128. [6] Edinger AL, Thompson CB. Death by design: apoptosis, necrosis and autophagy. Curr Opin Cell Biol, 2004, 16(6): 663–639. [7] Kroemer G, El-Deiry WS, Golstein P, Peter ME, Vaux D, Vandenabeele P, Zhivotovsky B, Blagosklonny MV, Malorni W, Knight RA, Piacentini M, Nagata S, Melino G. Classification of cell death: recommendations of the No-menclature Committee on Cell Death. Cell Death Differ, 2009, 16(1): 3–11. [8] Galluzzi L, Kroemer G. Necroptosis: A specialized path-way of programmed necrosis. Cell, 2008, 135(7): 1161–1163. [9] Rosenbaum DM, Degterev A, David J, Rosenbaum PS, Roth S, Grotta JC, Cuny GD, Yuan J, Savitz SI. Necrop-tosis, a novel form of caspase-independent cell death, contributes to neuronal damage in a retinal ische-mia-reperfusion injury model. J Neurosci Res, 2010, 88(7): 1569-1576. [10] Miao B, Degterev A. Methods to analyze cellular necrop-tosis. Methods Mol Biol, 2009, 559: 79–93. [11] Andrabi SA, Dawson TM, Dawson VL. Mitochondrial and nuclear cross talk in cell death: parthanatos. Ann N Y Acad Sci, 2008, 1147: 233–241. [12] Dawson VL, Dawson TM. Deadly conversations: nu-clear-mitochondrial cross-talk. J Bioenerg Biomembr, 2004, 36(4): 287–294. [13] Wang Y, Dawson VL, Dawson TM. Poly(ADP-ribose) signals to mitochondrial AIF: A key event in parthanatos. Exp Neurol, 2009, 218(2): 193–202. [14] Alano CC, Tran A, Tao R, Ying W, Karliner JS, Swanson RA. Differences among cell types in NAD(+) compartmentaliza-tion: A comparison of neurons, astrocytes, and cardiac myo-cytes. J Neurosci Res, 2007, 85(15): 3378–3385. [15] Koh DW, Lawler AM, Poitras MF, Sasaki M, Wattler S, Nehls MC, Stöger T, Poirier GG, Dawson VL, Dawson TM. Failure to degrade poly(ADP-ribose) causes increased sensitivity to cytotoxicity and early embryonic lethality. Proc Natl Acad Sci USA, 2004, 101(51): 17699–17704. [16] Polster BM, Basañez G, Etxebarria A, Hardwick JM, Nicholls DG. Calpain I induces cleavage and release of apoptosis-inducing factor from isolated mitochondria. J Biol Chem, 2005, 280(8): 6447–6454. [17] Cao G, Xing J, Xiao X, Liou AK, Gao Y, Yin XM, Clark RS, Graham SH, Chen J. Critical role of calpain I in mi-tochondrial release of apoptosis-inducing factor in ischemic neuronal injury. J Neurosci, 2007, 27(35): 9278–9293. [18] Moubarak RS, Yuste VJ, Artus C, Bouharrour A, Greer PA, Menissier-de Murcia J, Susin SA. Sequential activation of poly(ADP-ribose) polymerase 1, calpains, and Bax is es-sential in apoptosis-inducing factor-mediated programmed necrosis. Mol Cell Biol, 2007, 27(13): 4844–4862. [19] Vosler PS, Sun D, Wang S, Gao Y, Kintner DB, Signore AP, Cao G, Chen J. Calcium dysregulation induces apop-tosis-inducing factor release: cross-talk between PARP-1- and calpain-signaling pathways. Exp Neurol, 2009, 218(2): 213–220. [20] Wang
Outlines

/