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Cell density modulates apoptosis in human articular chondrocytes
1Division of Arthritis Research, The Scripps Research Institute, La Jolla, California 92037, USA.
Journal of Cellular Physiology
|August 3, 1999
Summary
Cell density significantly impacts CD95 and CD95L expression and apoptosis in human chondrocytes. Low density activates protective mechanisms, while high density increases susceptibility to CD95-mediated cell death.
Area of Science:
- Cell Biology
- Immunology
- Biochemistry
Background:
- CD95 (APO-1/Fas) and CD95 Ligand (CD95L) are key mediators of apoptosis.
- Human articular chondrocytes play a role in joint homeostasis and disease.
Purpose of the Study:
- To investigate the influence of cell density and serum on CD95/CD95L expression.
- To determine the impact of these factors on CD95-dependent apoptosis in chondrocytes.
Main Methods:
- Primary human articular chondrocytes cultured under varying densities (subconfluent vs. confluent).
- Flow cytometry used to assess CD95 and CD95L surface expression.
- CD95 agonistic antibody used to induce apoptosis; assessed with and without serum withdrawal.
Main Results:
- CD95 and CD95L expression decreased with increasing cell density.
- Apoptosis induction by CD95 antibody was significantly higher in confluent cultures.
- Serum withdrawal reduced CD95-dependent apoptosis in confluent but not subconfluent cultures.
Conclusions:
- Cell density is a critical regulator of CD95/CD95L expression in chondrocytes.
- Low cell density promotes anti-apoptotic mechanisms, while high density enhances susceptibility to CD95-mediated apoptosis.
- Serum availability further modulates apoptosis sensitivity in a density-dependent manner.