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

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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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Autores principales:	Costas, M.A., Müller Igaz, L., Holsboer, F., Arzt, E.
Formato:	Artículo publishedVersion
Lenguaje:	Inglés
Publicado:	2000
Materias:	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
Acceso en línea:	http://hdl.handle.net/20.500.12110/paper_01674889_v1499_n1-2_p122_Costas
Aporte de:	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires

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spelling	paperaa:paper_01674889_v1499_n1-2_p122_Costas2023-06-12T16:46:57Z Transrepression of NF-κB is not required for glucocorticoid-mediated protection of TNF-α-induced apoptosis on fibroblasts Biochim. Biophys. Acta Mol. Cell Res. 2000;1499(1-2):122-129 Costas, M.A. Müller Igaz, L. Holsboer, F. Arzt, E. 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 glucocorticoid glucocorticoid receptor I kappa B immunoglobulin enhancer binding protein NF kappaB inhibitor alpha NF-kappaB inhibitor alpha tumor necrosis factor 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 Apoptosis Cell Line DNA-Binding Proteins Fibroblasts Glucocorticoids I-kappa B Proteins Mice NF-kappa B Receptors, Glucocorticoid Transfection Tumor Necrosis Factor-alpha 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. Fil:Costas, M.A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Müller Igaz, L. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. 2000 info:eu-repo/semantics/article info:ar-repo/semantics/artículo info:eu-repo/semantics/publishedVersion application/pdf eng info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar http://hdl.handle.net/20.500.12110/paper_01674889_v1499_n1-2_p122_Costas
institution	Universidad de Buenos Aires
institution_str	I-28
repository_str	R-134
collection	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
language	Inglés
orig_language_str_mv	eng
topic	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 glucocorticoid glucocorticoid receptor I kappa B immunoglobulin enhancer binding protein NF kappaB inhibitor alpha NF-kappaB inhibitor alpha tumor necrosis factor 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 Apoptosis Cell Line DNA-Binding Proteins Fibroblasts Glucocorticoids I-kappa B Proteins Mice NF-kappa B Receptors, Glucocorticoid Transfection Tumor Necrosis Factor-alpha
spellingShingle	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 glucocorticoid glucocorticoid receptor I kappa B immunoglobulin enhancer binding protein NF kappaB inhibitor alpha NF-kappaB inhibitor alpha tumor necrosis factor 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 Apoptosis Cell Line DNA-Binding Proteins Fibroblasts Glucocorticoids I-kappa B Proteins Mice NF-kappa B Receptors, Glucocorticoid Transfection Tumor Necrosis Factor-alpha Costas, M.A. Müller Igaz, L. Holsboer, F. Arzt, E. Transrepression of NF-κB is not required for glucocorticoid-mediated protection of TNF-α-induced apoptosis on fibroblasts
topic_facet	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 glucocorticoid glucocorticoid receptor I kappa B immunoglobulin enhancer binding protein NF kappaB inhibitor alpha NF-kappaB inhibitor alpha tumor necrosis factor 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 Apoptosis Cell Line DNA-Binding Proteins Fibroblasts Glucocorticoids I-kappa B Proteins Mice NF-kappa B Receptors, Glucocorticoid Transfection Tumor Necrosis Factor-alpha
description	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.
format	Artículo Artículo publishedVersion
author	Costas, M.A. Müller Igaz, L. Holsboer, F. Arzt, E.
author_facet	Costas, M.A. Müller Igaz, L. Holsboer, F. Arzt, E.
author_sort	Costas, M.A.
title	Transrepression of NF-κB is not required for glucocorticoid-mediated protection of TNF-α-induced apoptosis on fibroblasts
title_short	Transrepression of NF-κB is not required for glucocorticoid-mediated protection of TNF-α-induced apoptosis on fibroblasts
title_full	Transrepression of NF-κB is not required for glucocorticoid-mediated protection of TNF-α-induced apoptosis on fibroblasts
title_fullStr	Transrepression of NF-κB is not required for glucocorticoid-mediated protection of TNF-α-induced apoptosis on fibroblasts
title_full_unstemmed	Transrepression of NF-κB is not required for glucocorticoid-mediated protection of TNF-α-induced apoptosis on fibroblasts
title_sort	transrepression of nf-κb is not required for glucocorticoid-mediated protection of tnf-α-induced apoptosis on fibroblasts
publishDate	2000
url	http://hdl.handle.net/20.500.12110/paper_01674889_v1499_n1-2_p122_Costas
work_keys_str_mv	AT costasma transrepressionofnfkbisnotrequiredforglucocorticoidmediatedprotectionoftnfainducedapoptosisonfibroblasts AT mullerigazl transrepressionofnfkbisnotrequiredforglucocorticoidmediatedprotectionoftnfainducedapoptosisonfibroblasts AT holsboerf transrepressionofnfkbisnotrequiredforglucocorticoidmediatedprotectionoftnfainducedapoptosisonfibroblasts AT arzte transrepressionofnfkbisnotrequiredforglucocorticoidmediatedprotectionoftnfainducedapoptosisonfibroblasts
_version_	1769810113946714112

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

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