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Cell-adhesion to crystal surfaces. Adhesion-induced physiological cell death
D Hanein1, A Yarden, H Sabanay
1Department of Structural Biology, Weizmann Institute of Science, Rehovot, Israel.
Cell Adhesion and Communication
|November 1, 1996
Summary
Cultured epithelial cells rapidly adhere to calcium tartrate crystals, but this interaction leads to cell death. Impaired cell motion and lack of proper extracellular matrix contacts trigger this physiological cell death.
Area of Science:
- Cell Biology
- Biophysics
- Materials Science
Background:
- Cultured epithelial cells exhibit rapid, stereospecific adhesion to calcium (R,R)-tartrate tetrahydrate crystals.
- This adhesion is proposed as an exaggerated model of initial cell attachment to tissue culture surfaces.
- Unlike normal cell attachment, this interaction results in massive cell death, not cell spreading or focal adhesion development.
Purpose of the Study:
- To characterize the fate of epithelial cells bound to calcium tartrate crystals.
- To investigate the mechanisms underlying crystal-induced cell death.
- To determine if direct crystal-cell interaction triggers lethal signals or if impaired adhesion dynamics are responsible.
Main Methods:
- Electron microscopy for ultrastructural analysis of crystal-bound cells.
- Flow cytometry to assess cell viability and death characteristics.
- Microscopic morphometry to quantify cellular changes.
- Analysis of transmembrane signaling pathways.
Main Results:
- Crystal-bound cells exhibited characteristics of physiological cell death.
- Direct interaction with the crystal surface did not directly trigger lethal transmembrane signals.
- Excessive cell-crystal interactions impaired cell motion, hindering RGD-dependent cell adhesion.
Conclusions:
- The massive cell death is not caused by direct lethal signaling from the crystal surface.
- Impaired cell motion and the inability to form proper extracellular matrix (ECM)-receptor contacts are implicated in triggering physiological cell death.
- This suggests that the deprivation of normal cell-matrix interactions can lead to programmed cell death in substrate-attached epithelial cells.