Rapid and significant induction of TRAIL-mediated type II cells in apoptosis of primary salivary epithelial cells in primary Sjögren's syndrome

Apoptosis. 2008 Nov;13(11):1322-30. doi: 10.1007/s10495-008-0261-2.

Abstract

Expressions of the effector molecules of Fas-mediated apoptosis in primary cultured salivary gland epithelial cells (SGEC) of primary Sjögren's syndrome (pSS) remain to be clarified. We focused on Fas-mediated caspase cleavage compared to tumor necrosis factor-related apoptosis inducing ligand (TRAIL)-mediated apoptosis. Induction of apoptosis was performed by anti-Fas antibody coupled with PI3K inhibitor, or TRAIL. Activation of caspases, cytochrome C, and apoptotic protease activating factor-1 (Apaf-1) was determined by western blotting or immunofluorescence observed by confocal microscopy. Fas-mediated apoptosis and activation of caspase 3/8 were induced in the presence of LY294002. TRAIL-induced apoptosis in SGEC, which was stronger than that induced by anti-Fas antibody. TRAIL-induced caspase 9 cleavage accompanied by activation of cytochrome C and Apaf-1 were not mediated by anti-Fas antibody. Our results suggest that death receptor-dependent apoptosis in primary cultured SGEC is regulated by the engagement of type II cells in pSS.

MeSH terms

  • Adult
  • Aged
  • Apoptosis*
  • Cells, Cultured
  • Epithelial Cells / metabolism*
  • Female
  • Gene Expression Regulation*
  • Humans
  • Microscopy, Confocal
  • Middle Aged
  • Models, Biological
  • Salivary Glands / metabolism*
  • Sjogren's Syndrome / genetics
  • Sjogren's Syndrome / metabolism
  • TNF-Related Apoptosis-Inducing Ligand / metabolism*
  • fas Receptor / metabolism

Substances

  • TNF-Related Apoptosis-Inducing Ligand
  • fas Receptor