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Serum withdrawal-induced apoptosis in thyroid cells is caused by loss of fibronectin-integrin interaction
T Di Matola1, F Mueller, G Fenzi
1Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università Federico II, Naples, Italy.
Abstract:
In some cell types, including a fetal thyroid cell line, denial of adhesion to extracellular matrix induces a type of apoptosis called anoikis. Serum withdrawal in dog and transformed rat thyroid cells also induces programmed cell death. Because serum can stimulate cells to produce some components of the extracellular matrix, it was of interest to determine the role of the matrix in the apoptosis induced by serum withdrawal in normal human thyroid cells in primary culture. The present report demonstrates that thyroid cells selectively produce and deposit insoluble fibronectin (FN) only when stimulated by serum. Adhesion in the presence of serum is dependent upon integrin-FN interaction. Serum withdrawal determines a degradation of the insoluble FN deposited and a detachment of the cells from the plates. In these conditions, cells undergo anoikis, demonstrated by DNA fragmentation and annexin V staining. Apoptosis was prevented by exogenous FN immobilized onto the plates. These results indicate that serum withdrawal induces apoptosis in human thyroid cells, determining FN degradation and loss of cell-matrix adhesion.
Insights
Serum withdrawal induces anoikis, a form of apoptosis, in human thyroid cells by degrading fibronectin and disrupting cell-matrix adhesion. Adding fibronectin prevents this programmed cell death.
Area of Science:
- Cell Biology
- Molecular Biology
- Biochemistry
Background:
- Anoikis, a form of apoptosis, is triggered by the loss of cell adhesion to the extracellular matrix in certain cell types.
- Serum withdrawal can induce programmed cell death in various thyroid cell lines.
- The role of the extracellular matrix in serum withdrawal-induced apoptosis in normal human thyroid cells requires investigation.
Purpose of the Study:
- To determine the role of the extracellular matrix in serum withdrawal-induced apoptosis in normal human thyroid cells in primary culture.
- To investigate the mechanism by which serum withdrawal affects cell-matrix adhesion and subsequent apoptosis.
Main Methods:
- Primary human thyroid cells were cultured under serum-stimulated and serum-deprived conditions.
- Production and deposition of insoluble fibronectin (FN) were assessed.
- Cell adhesion was evaluated based on integrin-FN interactions.
- Apoptosis was quantified using DNA fragmentation and annexin V staining.
- The effect of exogenous immobilized FN on apoptosis was examined.
Main Results:
- Serum stimulation induced selective production and deposition of insoluble fibronectin (FN) by thyroid cells.
- Cell adhesion in the presence of serum relied on integrin-FN interactions.
- Serum withdrawal led to degradation of deposited FN and cell detachment.
- Cells undergoing detachment and FN degradation exhibited anoikis, confirmed by DNA fragmentation and annexin V staining.
- Supplementation with exogenous immobilized FN prevented serum withdrawal-induced apoptosis.
Conclusions:
- Serum withdrawal triggers apoptosis in normal human thyroid cells.
- This apoptosis is mediated by the degradation of fibronectin and subsequent loss of cell-matrix adhesion.
- Fibronectin plays a crucial role in maintaining thyroid cell survival under serum-deprived conditions.