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Published on: January 31, 2012

Tumor necrosis factor-related apoptosis-inducing ligand induces apoptosis in human articular chondrocytes in vitro

I Pettersen1, Y Figenschau, E Olsen

  • 1Department of Experimental Pathology, Medical Faculty, University of Tromsö, N-9037 Tromsö, Norway.

Biochemical and Biophysical Research Communications
|August 15, 2002
PubMed

Insights

Normal human articular chondrocytes undergo apoptosis when exposed to Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL). This suggests TRAIL

Area of Science:

  • Immunology
  • Cell Biology
  • Rheumatology

Background:

  • Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is crucial for tumor surveillance via apoptosis.
  • TRAIL interacts with death receptors (DR4, DR5) and decoy receptors (DcR1, DcR2).

Purpose of the Study:

  • To investigate the susceptibility of normal human articular chondrocytes to TRAIL-mediated apoptosis.
  • To determine the expression of TRAIL receptors in chondrocytes.

Main Methods:

  • Reverse transcriptase-polymerase chain reaction (RT-PCR) to detect gene expression.
  • Flow cytometry to analyze cell surface receptor expression.
  • Assessment of cell death and caspase-3 activity following TRAIL treatment.

Main Results:

  • Normal human articular chondrocytes express apoptosis-mediating receptors (DR4, DR5) and a decoy receptor (DcR2).
  • Chondrocytes exhibited dose-dependent cell death upon TRAIL challenge.
  • Apoptotic morphology and active caspase-3 were observed in treated chondrocytes.

Conclusions:

  • Normal human articular chondrocytes are susceptible to TRAIL-induced apoptosis.
  • TRAIL signaling and its receptors may play a role in cartilage homeostasis and pathology.

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