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|Title:||TNF receptor deficiency reveals a translational control mechanism for adriamycin-induced Fas expression in cardiac tissues|
|Authors:||Yu Chin Lien|
Daret K. St. Clair
University of Kentucky College of Medicine
|Keywords:||Biochemistry, Genetics and Molecular Biology;Immunology and Microbiology;Medicine|
|Citation:||Cytokine. Vol.33, No.4 (2006), 226-230|
|Abstract:||Adriamycin, ADR, a potent chemotherapeutic agent, has been demonstrated to cause cardiomyocyte apoptosis, in part, via the Fas/Fas ligand-mediated cell death pathway. Our previous studies suggested that TNF-α receptors may mediate cardioprotection against ADR toxicity by the suppression of the Fas-mediated pathway. However, the role of TNF-α receptors in this process is unclear. In the present study, we extended our initial observation to determine the molecular mechanisms by which ADR induced Fas expression in the presence and absence of TNF receptors. Our results demonstrated that ADR-mediated p53 and AP-1 interaction and increased Fas mRNA levels independent of TNF receptors. However, the levels of Fas proteins only increased in the cardiac tissues of TNF receptor-deficient mice. These results demonstrated that the suppression of ADR-induced Fas expression by TNF receptors was not regulated at transcriptional levels, but may be regulated at a translational level. © 2006 Elsevier Ltd. All rights reserved.|
|Appears in Collections:||Scopus 2006-2010|
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