Transrepression of NF-κB is not required for glucocorticoid-mediated protection of TNF-α-induced apoptosis on fibroblasts

The cellular resistance to tumor necrosis factor (TNF) of most cell types has been attributed to both a protective pathway induced by this cytokine and the preexistence of protective factors in the target cell. NF-κB has been postulated as one of the principal factors involved in antiapoptotic gene...

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Detalles Bibliográficos
Autores: Costas, M.A., Müller Igaz, L., Holsboer, F., Arzt, E.
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2000
País:Argentina
Institución:Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturales
Repositorio:Biblioteca Digital (UBA-FCEN)
Idioma:inglés
OAI Identifier:paperaa:paper_01674889_v1499_n1-2_p122_Costas
Acceso en línea:http://hdl.handle.net/20.500.12110/paper_01674889_v1499_n1-2_p122_Costas
Access Level:acceso abierto
Palabra clave:Apoptosis
Glucocorticoid
Glucocorticoid receptor
Nuclear factor-κB
Tumor necrosis factor
beta galactosidase
dexamethasone
glucocorticoid
glucocorticoid receptor
I kappa B
immunoglobulin enhancer binding protein
luciferase
messenger RNA
tumor necrosis factor alpha
tumor necrosis factor alpha receptor
DNA binding protein
NF kappaB inhibitor alpha
NF-kappaB inhibitor alpha
animal cell
apoptosis
article
cell protection
controlled study
cytotoxicity
fibroblast
gene expression regulation
gene repression
mouse
nonhuman
priority journal
protein expression
suppressor cell
target cell destruction
transactivation
animal
biosynthesis
cell line
drug antagonism
genetic transfection
metabolism
Animals
Cell Line
DNA-Binding Proteins
Fibroblasts
Glucocorticoids
I-kappa B Proteins
Mice
NF-kappa B
Receptors, Glucocorticoid
Transfection
Tumor Necrosis Factor-alpha
Descripción
Sumario:The cellular resistance to tumor necrosis factor (TNF) of most cell types has been attributed to both a protective pathway induced by this cytokine and the preexistence of protective factors in the target cell. NF-κB has been postulated as one of the principal factors involved in antiapoptotic gene expression control on TNF-resistant cells. We have previously shown that glucocorticoids protect the naturally TNF-sensitive L-929 cells from apoptosis. Here we analyze the role of NF-κB and glucocorticoids on TNF-induced apoptosis in L-929 cells. We found that inhibition of NF-κB enhanced the sensitivity to TNF-induced apoptosis. Glucocorticoids inhibited NF-κB transactivation via IκB induction. Moreover, glucocorticoids protected from TNF-induced apoptosis even when NF-κB activity was inhibited by stable or transient expression of the superrepressor IκB. These results demonstrate that although glucocorticoids inhibit NF-κB transactivation in these cells, this is not required for their protection from TNF-induced apoptosis. (C) 2000 Elsevier Science B.V.