Tumor necrosis factor (TNF) up-regulates the expression of p75 but not p55 TNF receptors, and both receptors mediate, independently of each other, up-regulation of transforming growth factor alpha and epidermal growth factor receptor mRNA

J Biol Chem. 1993 Feb 5;268(4):2762-6.

Abstract

The expression and cytokine-mediated regulation of the two different receptors for tumor necrosis factor, TNF-R-75 and TNF-R-55, was investigated in human malignant epithelial cell lines. Here we show that cells treated with TNF-alpha up-regulate the TNF-R-75 mRNA and protein levels. No changes were seen regarding the level of TNF-R-55 transcripts. Phospholipase and protein kinase C inhibitors abrogated the signal transduction pathway of TNF-mediated TNF-R-75 mRNA up-regulation which proceeded in the absence of transcriptional activation. This process was also elicited by an agonistic antibody binding specifically to TNF-R-55. Ligand binding assays using specific inhibitory antibodies showed a marked shift in active binding sites from p55 to p75 without significant changes in the total binding for TNF-alpha after up-regulation of p75 TNF-R. This ligand-induced regulation of one of the corresponding receptors has so far only been detected in malignant epithelial cells and not in hematopoietic cell lines. In our search for a specific function we were able to show that p75 is the specific receptor for TNF-mediated up-regulation of transforming growth factor alpha mRNA, whereas p55 is the signal transducer for TNF-induced up-regulation of epidermal growth factor receptor mRNA. This is the first demonstration of an exclusive function of TNF-R-75 in cells of epithelial origin.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • ErbB Receptors / genetics*
  • Gene Expression Regulation / drug effects
  • Genes, fos
  • Humans
  • In Vitro Techniques
  • Molecular Weight
  • Phospholipases / metabolism
  • Protein Kinases / metabolism
  • RNA, Messenger / genetics
  • Receptors, Cell Surface / genetics
  • Receptors, Cell Surface / metabolism*
  • Receptors, Tumor Necrosis Factor
  • Signal Transduction
  • Solubility
  • Transcription, Genetic
  • Transforming Growth Factor alpha / genetics*
  • Transforming Growth Factor alpha / metabolism
  • Tumor Cells, Cultured
  • Tumor Necrosis Factor-alpha / pharmacology*
  • Up-Regulation

Substances

  • RNA, Messenger
  • Receptors, Cell Surface
  • Receptors, Tumor Necrosis Factor
  • Transforming Growth Factor alpha
  • Tumor Necrosis Factor-alpha
  • Protein Kinases
  • ErbB Receptors
  • Phospholipases