Skip Navigation

Cardiovascular Research 2004 63(4):682-688; doi:10.1016/j.cardiores.2004.04.018
© 2004 by European Society of Cardiology
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Chen, M.
Right arrow Articles by Szabó, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Chen, M.
Right arrow Articles by Szabó, C.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2004, European Society of Cardiology

Mitochondrial-to-nuclear translocation of apoptosis-inducing factor in cardiac myocytes during oxidant stress: potential role of poly(ADP-ribose) polymerase-1

Min Chen, Zsuzsanna Zsengellér, Chun-Yang Xiao and Csaba Szabó*

Inotek Pharmaceuticals Corporation, Suite 419E, 100 Cummings Center, Beverly, MA 01915, USA

* Corresponding author. Tel.: +1-978-232-9660; fax: +1-978-232-8975. Email address: szabocsaba{at}aol.com

Objective: Oxidant stress-induced activation of poly(ADP-ribose) polymerase (PARP) plays a role in the pathogenesis of various cardiovascular diseases. We have now investigated the role of PARP in the death of cardiac myocytes in response to oxidant stress induced by hydrogen peroxide, with focus on the mitochondrial function. Methods and results: Using wild-type and PARP-1-deficient murine myocytes challenged with hydrogen peroxide, we found that mitochondrial respiration and mitochondrial membrane potential were better preserved in PARP-deficient myocytes and cellular NAD+ levels were maintained. The release of the mitochondrial cell death factor cytochrome c, and the mitochondrial-to-nuclear translocation of apoptosis-inducing factor (AIF) were also attenuated in the PARP-deficient myocytes. Conclusion: PARP-1, directly or indirectly, regulates the translocation of AIF in myocytes subjected to oxidative stress. The current results are consistent with the view that PARP-1 activation, via induction of mitochondrial dysfunction and promotion of mitochondrial cell death pathways, plays a deleterious pathophysiological role under conditions of oxidative stress.

KEYWORDS Oxidative stress; DNA; Apoptosis; Necrosis; Heart

Time for primary review 28 days


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Cardiovasc ResHome page
S. Choudhury, S. Bae, S. R. Kumar, Q. Ke, B. Yalamarti, J. H. Choi, L. A. Kirshenbaum, and P. M. Kang
Role of AIF in cardiac apoptosis in hypertrophic cardiomyocytes from Dahl salt-sensitive rats
Cardiovasc Res, August 14, 2009; (2009) cvp261v2.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
S. Miyamoto, M. Rubio, and M. A. Sussman
Nuclear and mitochondrial signalling Akts in cardiomyocytes
Cardiovasc Res, May 1, 2009; 82(2): 272 - 285.
[Abstract] [Full Text] [PDF]

Home page
 DiabetesHome page
C. Szabo, A. Biser, R. Benko, E. Bottinger, and K. Susztak
Poly(ADP-Ribose) Polymerase Inhibitors Ameliorate Nephropathy of Type 2 Diabetic Leprdb/db Mice
Diabetes, November 1, 2006; 55(11): 3004 - 3012.
[Abstract] [Full Text] [PDF]

Home page
 Microbiol. Mol. Biol. Rev.Home page
P. O. Hassa, S. S. Haenni, M. Elser, and M. O. Hottiger
Nuclear ADP-Ribosylation Reactions in Mammalian Cells: Where Are We Today and Where Are We Going?
Microbiol. Mol. Biol. Rev., September 1, 2006; 70(3): 789 - 829.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
A. Tapodi, B. Debreceni, K. Hanto, Z. Bognar, I. Wittmann, F. Gallyas Jr., G. Varbiro, and B. Sumegi
Pivotal Role of Akt Activation in Mitochondrial Protection and Cell Survival by Poly(ADP-ribose)polymerase-1 Inhibition in Oxidative Stress
J. Biol. Chem., October 21, 2005; 280(42): 35767 - 35775.
[Abstract] [Full Text] [PDF]

Home page
 Circ. Res.Home page
V. P.M. van Empel, A. T. Bertrand, R. van der Nagel, S. Kostin, P. A. Doevendans, H. J. Crijns, E. de Wit, W. Sluiter, S. L. Ackerman, and L. J. De Windt
Downregulation of Apoptosis-Inducing Factor in Harlequin Mutant Mice Sensitizes the Myocardium to Oxidative Stress-Related Cell Death and Pressure Overload-Induced Decompensation
Circ. Res., June 24, 2005; 96(12): e92 - e101.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
G. Cipriani, E. Rapizzi, A. Vannacci, R. Rizzuto, F. Moroni, and A. Chiarugi
Nuclear Poly(ADP-ribose) Polymerase-1 Rapidly Triggers Mitochondrial Dysfunction
J. Biol. Chem., April 29, 2005; 280(17): 17227 - 17234.
[Abstract] [Full Text] [PDF]

Home page
 J. Pharmacol. Exp. Ther.Home page
C.-Y. Xiao, M. Chen, Z. Zsengeller, H. Li, L. Kiss, M. Kollai, and C. Szabo
Poly(ADP-Ribose) Polymerase Promotes Cardiac Remodeling, Contractile Failure, and Translocation of Apoptosis-Inducing Factor in a Murine Experimental Model of Aortic Banding and Heart Failure
J. Pharmacol. Exp. Ther., March 1, 2005; 312(3): 891 - 898.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.