Dexamethasone inhibits apoptosis in C6 glioma cells through increased expression of Bcl-XL
- First Online:
- Cite this article as:
- Ní Chonghaile, T., Concannon, C.G., Szegezdi, E. et al. Apoptosis (2006) 11: 1247. doi:10.1007/s10495-006-7233-1
- 148 Downloads
The glucocorticoid dexamethasone (Dex) has been reported to modulate a number of signaling pathways and physiological processes, including apoptosis. This study was carried out to investigate the cytoprotective mechanism of Dex in C6 glioma cells. Pre-treatment of cells with Dex inhibited apoptosis induced by staurosporine, etoposide and thapsigargin. Apoptosis inhibition correlated with blockade of mitochondrial cytochrome c release, abolition of caspase-3 activity along with inhibition of caspase-9 and PARP cleavage. Dex-mediated cytoprotection coincided with the induction of the anti-apoptotic protein, Bcl-XL. The specific glucocorticoid receptor antagonist, RU486, reversed the anti-apoptotic effect of Dex and prevented Bcl-XL induction. Here, we show for the first time that knockdown of Bcl-XL expression with siRNA reversed the protective effects of the glucocorticoid in glioma cells. We conclude that Dex-mediated inhibition of apoptosis in C6 glioma cells is through induction of Bcl-XL.
Glyceraldehyde 3-phosphate dehydrogenase
Glucocorticoid response element