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Originally published In Press as doi:10.1074/jbc.M108645200 on October 8, 2001

J. Biol. Chem., Vol. 276, Issue 50, 47518-47523, December 14, 2001
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Vibrio vulnificus Cytolysin Induces Superoxide Anion-initiated Apoptotic Signaling Pathway in Human ECV304 Cells*

Kang-Beom KwonDagger , Jeong-Yeh Yang§, Do-Gon RyuDagger , Hye-Won Rho§, Jong-Suk Kim§, Jin-Woo Park§, Hyung-Rho Kim§, and Byung-Hyun Park§

From the Dagger  Department of Physiology, School of Oriental Medicine, Won-Kwang University, Iksan 570-749, and the § Department of Biochemistry and Institute for Medical Sciences, Chonbuk National University Medical School, Chonju, 561-756 Republic of Korea

Previous studies showed that exposure to Vibrio vulnificus cytolysin (VVC) caused characteristic morphologic changes and dysfunction of vascular structures in lung. VVC showed cytotoxicity for mammalian cells in culture and acted as a vascular permeability factor. In this study, the underlying mechanisms of VVC-induced cytotoxicity was investigated on ECV304 cell, a human vascular endothelial cell line. When cells were exposed to 0.4 hemolytic units (HU) of VVC, consecutive apoptotic events were observed; the elevation of superoxide anion (O&cjs1138;2), the release of cytochrome c, the activation of caspase-3, the cleavage of poly(ADP-ribose) polymerase, and the DNA fragmentation. The pretreatment with 4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl (TEMPO), O&cjs1138;2 scavenger, completely abolished O&cjs1138;2 levels and downstream apoptotic events. Moreover, pretreatment with cyclosporin A (CsA), a mitochondrial permeability transition inhibitor, was capable of attenuating O&cjs1138;2-mediated cytochrome c release and caspase-3 activation, and consequent apoptosis. Apoptosis, as demonstrated by oligonucleosomal DNA fragmentation and fluorescence microscopy, was induced 24 h after VVC treatment, which was also prevented by caspase-3 inhibitor, Ac-DEVD-CHO. Caspase-1 inhibitor, Ac-YVAD-CHO, did not protect ECV 304 cells from apoptosis. These results suggest a scenario where VVC-induced apoptosis is triggered by the generation of O&cjs1138;2, release of cytochrome c from mitochondria, activation of caspase-3, degradation of poly(ADP-ribose) polymerase, and DNA fragmentation. The induction of apoptosis in endothelial cells by VVC may provide a pivotal mechanism for understanding the pathophysiology of septicemia.

* This work was supported in part by Grant 2001-1-20500-012-1 from the Basic Research Program of the Korea Science & Engineering Foundation and Chonbuk National University Post-doc Training Program (to J. Y. Yang).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

To whom correspondence should be addressed: Dept. of Biochemistry, Chonbuk National University Medical School, Chonju, 561-756 Republic of Korea. Tel.: 82-63-270-3139; Fax: 82-63-274-9833; E-mail: bhpark@moak.chonbuk.ac.kr.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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