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Title: Tumor necrosis factor receptor deficiency exacerbated Adriamycin-induced cardiomyocytes apoptosis: An insight into the Fas connection
Authors: Yu Chin Lien
Shu Mei Lin
Ramaneeya Nithipongvanitch
Terry D. Oberley
Teresa Noel
Qing Zhao
Chotiros Daosukho
Daret K. St. Clair
University of Kentucky College of Medicine
University of Wisconsin Madison
Mahidol University
Columbia University, College of Physicians and Surgeons
Chung Hwa College of Medical Technology Taiwan
Guangzhou Medical University
Keywords: Biochemistry, Genetics and Molecular Biology;Medicine
Issue Date: 1-Feb-2006
Citation: Molecular Cancer Therapeutics. Vol.5, No.2 (2006), 261-269
Abstract: Cardiomyopathy is a major dose-limiting factor for applications of Adriamycin, a potent chemotherapeutic agent. The present study tested the hypothesis that increased tumor necrosis factor (TNF)-α signaling via its receptors protects against Adriamycin-induced cardiac injury. We used mice in which both TNF receptor I and II have been selectively inactivated (DKO) with wild-type mice as controls. Morphometric studies of cardiac tissue following Adriamycin treatment revealed greater ultrastructural damage in cardiomyocyte mitochondria from DKO mice. Biochemical studies of cardiac tissues showed cytochrome c release and the increase in proapoptotic protein levels, suggesting that lack of TNF-α receptor I and II exacerbates Adriamycin-induced cardiac injury. The protective role of TNF receptor I and II was directly confirmed in isolated primary cardiomyocytes. Interestingly, following Adriamycin treatment, the levels of Fas decreased in the wild-type mice. In contrast, DKO mice had an increase in Fas levels and its downstream target, mitochondrial truncated Bid. These results suggested that TNF-α receptors play a critical role in cardioprotection by suppression of the mitochondrial-mediated associated cell death pathway. Copyright © 2006 American Association for Cancer Research.
ISSN: 15357163
Appears in Collections:Scopus 2006-2010

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