Anti-obesity and anti-tumor pro-apoptotic peptides are sufficient to cause release of cytochrome c from vesicles

Sandoval, Cristina M.; Salzameda, Bridget; Reyes, Kristine; Williams, Taylor; Hohman, Valerie S.; Plesniak, Leigh A.

doi:10.1016/j.febslet.2007.10.051

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Volume 581, Issue 28 , Pages 5464-5468, 27 November 2007

Anti-obesity and anti-tumor pro-apoptotic peptides are sufficient to cause release of cytochrome c from vesicles

Edited by Robert Barouki

Department of Chemistry and Biochemistry, University of San Diego, 5998 Alcala Park, San Diego, CA 92110, USA

Received 30 August 2007; received in revised form 5 October 2007; accepted 27 October 2007. published online 05 November 2007.

Abstract

Peptides that target tissue for an apoptotic death have potential as therapeutics in a variety of disease conditions. The class of peptides described herein enters the cell through a specific receptor-mediated interaction. Once inside the cell, the peptide migrates toward the mitochondria, where the membrane barrier is disrupted. These experiments demonstrate that upon treatment with these short peptides large unilamellar vesicles are not lysed, a graded mode of leakage is observed and the transient pores formed by these peptides are large enough to release entrapped cytochrome c from the vesicles.

Abbreviations: FD4, fitc-dextran 4kDa, FD10, fitc-dextran 10kDa, FD20, fitc-dextran 20kDa, FD40, fitc-dextran 40kDa, FD70, fitc-dextran 70kDa, fitc, fluorescein isothiocyanate, HKP, hunter-killer peptide, LUVs, large unilamellar vesicles, Mst, mastoparan, PC, phosphatidylcholine, PG, phosphatidylglycerol, TNF, tumor necrosis factor, TRAIL, TNF-related apoptosis-inducing ligand