Tumor necrosis factor α stimulates sphingomyelinase through the 55 kDa receptor in HL-60 cells

Fumi Yanaga, Steve P. Watson

Research output: Contribution to journalArticle

55 Citations (Scopus)

Abstract

Tumor necrosis factor α (TNFα) stimulated rapid (seconds) hydrolysis of sphingomyelin in HL-60 cells, formation of phosphocholine (PCho) and a decrease in choline. The response to TNFα was concentration dependent with a maximal effect at 3-10 nM. The monoclonal antibody (mAb). htr-9, which behaves as an agonist at the 55 kDa subtype of the TNF receptor, also stimulated sphingomyelin hydrolysis in intact cells. In contrast, the mAb, utr-1, which behaves as an antagonist at the 75 kDa receptor subtype, had no effect on sphingomyelin hydrolysis either on its own or in the presence of TNFα. In addition, htr-9 or TNFα stimulated hydrolysis of sphingomyelin in a membrane fraction of HL-60 cells. These results are consistent with a role of sphinpomyelin hydrolysis as an early event in the signalling mechanism or TNFα, and suggest that this pathway is activated through the 55 kDa subtype of the TNF receptor.

Original languageEnglish
Pages (from-to)297-300
Number of pages4
JournalFEBS Letters
Volume314
Issue number3
DOIs
Publication statusPublished - Dec 21 1992

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

Fingerprint Dive into the research topics of 'Tumor necrosis factor α stimulates sphingomyelinase through the 55 kDa receptor in HL-60 cells'. Together they form a unique fingerprint.

  • Cite this