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Cardiovascular Research Advance Access first published online on July 24, 2009
This version [Corrected Proof] published online on August 14, 2009
Cardiovascular Research, doi:10.1093/cvr/cvp261
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

Role of AIF in cardiac apoptosis in hypertrophic cardiomyocytes from Dahl salt-sensitive rats

Sangita Choudhury1, Soochan Bae1, Sheetal R. Kumar1, Qingen Ke1, Bhargavi Yalamarti1, Jun H. Choi1, Lorrie A. Kirshenbaum2 and Peter M. Kang1,*

1 Cardiovascular Division, Beth Israel Deaconess Medical Center and Harvard Medical School, 3 Blackfan Circle, Rm 910, Boston, MA 02215, USA
2 Institute of Cardiovascular Sciences, University of Manitoba, Winnipeg, Manitoba, Canada

* Corresponding author. Tel: +1 617 735 4290, Fax: +1 617 735 4202, Email: pkang{at}bidmc.harvard.edu

Aims: The caspases are thought to be central mediators of the apoptotic program, but recent data indicate that apoptosis may also be mediated by caspase-independent mechanisms such as apoptosis-inducing factor (AIF). The role of AIF-induced apoptosis in heart, however, is currently not well understood. The aim of this study was to investigate the presence of and conditions for AIF-induced cardiac apoptosis in vitro.

Methods and results: Hypertrophic cardiomyocyte (H-CM) cultures were prepared from the hearts of Dahl salt-sensitive rats fed a high salt diet. Apoptotic stimulation induced by hypoxia/reoxygenation or staurosporine (1 µM) enhanced AIF release in H-CMs compared with non-hypertrophic cardiomyocytes (N-CMs). Caspase inhibition using zVAD.fmk (25 µM) or overexpression of CrmA using recombinant adenovirus only partially protected N-CMs from apoptosis (63 ± 0.93%) and provided no significant protection against apoptosis in hypertrophic cells (23 ± 1.03%). On the other hand, poly-ADP-ribose polymerase inhibition using 4-AN (20 µM) during apoptotic stimulation blocked the release of AIF from mitochondria and significantly improved cell viability in hypertrophied cardiomyocytes (74 ± 1.18%).

Conclusion: A caspase-dependent, apoptotic pathway is important for N-CM death, whereas a caspase-independent, AIF-mediated pathway plays a critical role in H-CMs.

KEYWORDS Apoptosis-inducing factor; Caspase; Cardiomyocytes; Hypertrophy; PARP

Time for primary review: 36 days


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