TNF receptor deficiency reveals a translational control mechanism for adriamycin-induced Fas expression in cardiac tissues

Yu Chin Lien, Chotiros Daosukho, Daret K. St. Clair

Research output: Contribution to journalArticlepeer-review

7 Scopus citations

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.

Original languageEnglish
Pages (from-to)226-230
Number of pages5
JournalCytokine
Volume33
Issue number4
DOIs
StatePublished - Feb 21 2006

Bibliographical note

Funding Information:
This work was partially supported by NIH grants CA 80152, CA 94853, and CA66239.

Keywords

  • AP-1
  • Adriamycin
  • Fas
  • TNF receptors
  • p53

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Biochemistry
  • Hematology
  • Molecular Biology

Fingerprint

Dive into the research topics of 'TNF receptor deficiency reveals a translational control mechanism for adriamycin-induced Fas expression in cardiac tissues'. Together they form a unique fingerprint.

Cite this