Peer-Reviewed Journal Details
Mandatory Fields
Ni Chonghaile, T,Concannon, CG,Szegezdi, E,Gorman, AM,Samali, A
2006
July
Apoptosis
Dexamethasone inhibits apoptosis in C6 glioma cells through increased expression of Bcl-X-L
Published
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Optional Fields
apoptosis Bcl-X-L dexamethasone glioma siRNA CYTOCHROME-C ENDOPLASMIC-RETICULUM GLUCOCORTICOID-RECEPTOR PARTIAL RESISTANCE MITOCHONDRIA BAX BCL-X(L) INDUCTION RELEASE DEATH
11
1247
1255
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-X-L. The specific glucocorticoid receptor antagonist, RU486, reversed the anti-apoptotic effect of Dex and prevented Bcl-X-L induction. Here, we show for the first time that knockdown of Bcl-X-L 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-X-L.
DOI 10.1007/s10495-006-7233-1
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