A molecular basis of cell death in olfactory epithelium

A I Farbman1, J A Buchholz, Y Suzuki

  • 1Department of Neurobiology and Physiology, Northwestern University, Evanston, Illinois 60208-3520, USA. afarbman@nwu.edu

Insights

The olfactory epithelium expresses Fas/FasL and TNF-alpha/TNFR1. Activating these pathways with Fas ligand or TNF-alpha increases apoptosis in olfactory epithelium cultures, suggesting their role in cell death.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Immunology

Background:

  • The Fas receptor/Fas ligand (FasL) and tumor necrosis factor receptor-1 (TNFR1)/TNF-alpha pathways are known initiators of apoptosis.
  • The olfactory epithelium is a complex sensory tissue with ongoing cell turnover.

Purpose of the Study:

  • To investigate the presence and potential role of Fas/FasL and TNF-alpha/TNFR1 signaling in the rat olfactory epithelium.
  • To determine if these pathways can induce apoptosis in olfactory epithelium cultures.

Main Methods:

  • Immunohistochemistry and Western blotting were used to detect Fas and FasL expression in rat olfactory epithelium.
  • Organotypic cultures of fetal rat olfactory epithelium were treated with FasL or TNF-alpha.
  • Apoptotic bodies were quantified after treatment.

Main Results:

  • mRNA for Fas/FasL and TNF-alpha/TNFR1 were detected in the unperturbed olfactory epithelium.
  • Fas and FasL proteins were localized to neurons and microvillar cells.
  • Exposure to FasL or TNF-alpha significantly increased apoptotic bodies in cultured olfactory epithelium.

Conclusions:

  • The Fas/FasL and TNF-alpha/TNFR1 signaling pathways are expressed in the rat olfactory epithelium.
  • These pathways are capable of inducing apoptosis in olfactory epithelium cells.
  • Fas/FasL and TNF-alpha/TNFR1 may play a role in regulating cell death within the olfactory epithelium.

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