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GM-CSF RESCUES TF-1 CELLS FROM GROWTH FACTOR WITHDRAWAL-INDUCED, BUT NOT DIFFERENTIATION-INDUCED APOPTOSIS: THE ROLE OF BCL-2 AND MCL-1
- Source :
- Cytokine; November 1999, Vol. 11 Issue: 11 p849-855, 7p
- Publication Year :
- 1999
-
Abstract
- Cytokines such as granulocyte–macrophage colony-stimulating factor (GM-CSF) and IL-3 promote the survival and stimulate the proliferation of haematopoietic cells. Using the GM-CSF-dependent TF-1 myeloid leukaemia cell line, the authors show that the endogenous levels of BCL-2 and MCL-1 are downregulated upon GM-CSF withdrawal, whereas the levels of BCL-xLand Bax are unchanged. Re-exposure of growth factor deprived cells to GM-CSF resulted in an early and transient increase in MCL-1 expression, and prolonged induction of BCL-2, which prevented apoptosis. In contrast, the expression of BCL-2 and MCL-1 were not modulated during TPA-induced differentiation of TF-1 cells, which was followed by apoptosis despite the presence of GM-CSF. TF-1 cells overexpressing BCL-2 or MCL-1 underwent delayed apoptosis upon growth factor withdrawal, but displayed no impaired apoptosis in response to TPA. Erythropoietin (Epo) induced the expression of BCL-2 and MCL-1 protein in TF-1 cells, however it did not support their long term proliferation, further demonstrating that upregulation of these anti-apoptotic genes is insufficient for the long term proliferation of TF-1 cells.
Details
- Language :
- English
- ISSN :
- 10434666 and 10960023
- Volume :
- 11
- Issue :
- 11
- Database :
- Supplemental Index
- Journal :
- Cytokine
- Publication Type :
- Periodical
- Accession number :
- ejs691604
- Full Text :
- https://doi.org/10.1006/cyto.1999.0514