CD95-mediated apoptosis in vivo involves acid sphingomyelinase. Academic Article uri icon

Overview

abstract

  • Acid sphingomyelinase (ASM) is reported to have an essential function in stress-induced apoptosis although the physiological function of ASM in receptor-triggered apoptosis is unknown. Here, we delineate a pivotal role for ASM in CD95-triggered apoptosis of peripheral lymphocytes or hepatocytes in vivo. We employed intravenous injection of anti-CD4 antibodies or phytohemagglutinin that was previously shown to result in apoptosis of peripheral blood lymphocytes or hepatocytes via the endogenous CD95/CD95 ligand system. Our results demonstrate a high susceptibility in normal mice whereas ASM knock-out mice fail to immunodeplete T cells or develop autoimmune-like hepatitis. Likewise, ASM-deficient mice or hepatocytes and splenocytes ex vivo manifest resistance to anti-CD95 treatment. These results provide in vivo evidence for an important physiological function of ASM in CD95-induced apoptosis.

publication date

  • September 1, 2000

Research

keywords

  • Apoptosis
  • Sphingomyelin Phosphodiesterase
  • fas Receptor

Identity

Scopus Document Identifier

  • 0034282716

PubMed ID

  • 10867001

Additional Document Info

volume

  • 275

issue

  • 35