TNF-alpha-induced apoptosis is prevented by erythropoietin treatment on SH-SY5Y cells

Autores
Pregi, Nicolás; Wenker, Shirley Denise; Vittori, Daniela Cecilia; Perez Leiros, Claudia; Nesse, Alcira Beatriz
Año de publicación
2009
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
The growth factor erythropoietin (Epo) has shown neuronal protective action in addition to its well known proerythroid activity. Furthermore, Epo has dealt with cellular inflammation by inhibiting the expression of several proinflammatory cytokines, such as IL-1 and TNF-α. The action of TNF can have both apoptotic and antiapoptotic consequences due to altered balance between different cell signalling pathways. This work has focused on the apoptotic effects of this cytokine and the potential protective action of Epo. The model we used was neuroblastoma SH-SY5Y cells cultured in the presence of 25 ng/ml TNF-α or pretreated with 25 U/ml Epo for 12 h before the addition of TNF-α. Apoptosis was evaluated by differential cell count after Hoechst staining, analysis of DNA ladder pattern, and measurement of caspase activity. Despite its ability to induce NF-κB nuclear translocation, TNF-α induced cell death, which was found to be associated to upregulation of TNF Receptor 1 expression. On the other hand, cells activated by Epo became resistant to cell death. Prevention of death receptor upregulation and caspase activation may explain this antiapoptotic effect of Epo, which may be also favoured by the induction of a higher expression of protective factors, such as Bcl-2 and NF-κB, through mechanisms involving Jak/STAT and PI3K signalling pathways. © 2008 Elsevier Inc. All rights reserved.
Fil: Pregi, Nicolás. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; Argentina
Fil: Wenker, Shirley Denise. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; Argentina
Fil: Vittori, Daniela Cecilia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; Argentina
Fil: Perez Leiros, Claudia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; Argentina
Fil: Nesse, Alcira Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; Argentina
Materia
Apoptosis
Erythropoietin
Inflammation
Neuroprotection
Nf-ΚB
Sh-Sy5y Cells
Tnf-Α
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/66372

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network_name_str CONICET Digital (CONICET)
spelling TNF-alpha-induced apoptosis is prevented by erythropoietin treatment on SH-SY5Y cellsPregi, NicolásWenker, Shirley DeniseVittori, Daniela CeciliaPerez Leiros, ClaudiaNesse, Alcira BeatrizApoptosisErythropoietinInflammationNeuroprotectionNf-ΚBSh-Sy5y CellsTnf-Αhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1The growth factor erythropoietin (Epo) has shown neuronal protective action in addition to its well known proerythroid activity. Furthermore, Epo has dealt with cellular inflammation by inhibiting the expression of several proinflammatory cytokines, such as IL-1 and TNF-α. The action of TNF can have both apoptotic and antiapoptotic consequences due to altered balance between different cell signalling pathways. This work has focused on the apoptotic effects of this cytokine and the potential protective action of Epo. The model we used was neuroblastoma SH-SY5Y cells cultured in the presence of 25 ng/ml TNF-α or pretreated with 25 U/ml Epo for 12 h before the addition of TNF-α. Apoptosis was evaluated by differential cell count after Hoechst staining, analysis of DNA ladder pattern, and measurement of caspase activity. Despite its ability to induce NF-κB nuclear translocation, TNF-α induced cell death, which was found to be associated to upregulation of TNF Receptor 1 expression. On the other hand, cells activated by Epo became resistant to cell death. Prevention of death receptor upregulation and caspase activation may explain this antiapoptotic effect of Epo, which may be also favoured by the induction of a higher expression of protective factors, such as Bcl-2 and NF-κB, through mechanisms involving Jak/STAT and PI3K signalling pathways. © 2008 Elsevier Inc. All rights reserved.Fil: Pregi, Nicolás. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; ArgentinaFil: Wenker, Shirley Denise. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; ArgentinaFil: Vittori, Daniela Cecilia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; ArgentinaFil: Perez Leiros, Claudia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; ArgentinaFil: Nesse, Alcira Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; ArgentinaElsevier Inc2009-02info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/66372Pregi, Nicolás; Wenker, Shirley Denise; Vittori, Daniela Cecilia; Perez Leiros, Claudia; Nesse, Alcira Beatriz; TNF-alpha-induced apoptosis is prevented by erythropoietin treatment on SH-SY5Y cells; Elsevier Inc; Experimental Cell Research; 315; 3; 2-2009; 419-4310014-4827CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/http://www.sciencedirect.com/science/article/pii/S0014482708004692info:eu-repo/semantics/altIdentifier/doi/10.1016/j.yexcr.2008.11.005info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:47:01Zoai:ri.conicet.gov.ar:11336/66372instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-03 09:47:01.342CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv TNF-alpha-induced apoptosis is prevented by erythropoietin treatment on SH-SY5Y cells
title TNF-alpha-induced apoptosis is prevented by erythropoietin treatment on SH-SY5Y cells
spellingShingle TNF-alpha-induced apoptosis is prevented by erythropoietin treatment on SH-SY5Y cells
Pregi, Nicolás
Apoptosis
Erythropoietin
Inflammation
Neuroprotection
Nf-ΚB
Sh-Sy5y Cells
Tnf-Α
title_short TNF-alpha-induced apoptosis is prevented by erythropoietin treatment on SH-SY5Y cells
title_full TNF-alpha-induced apoptosis is prevented by erythropoietin treatment on SH-SY5Y cells
title_fullStr TNF-alpha-induced apoptosis is prevented by erythropoietin treatment on SH-SY5Y cells
title_full_unstemmed TNF-alpha-induced apoptosis is prevented by erythropoietin treatment on SH-SY5Y cells
title_sort TNF-alpha-induced apoptosis is prevented by erythropoietin treatment on SH-SY5Y cells
dc.creator.none.fl_str_mv Pregi, Nicolás
Wenker, Shirley Denise
Vittori, Daniela Cecilia
Perez Leiros, Claudia
Nesse, Alcira Beatriz
author Pregi, Nicolás
author_facet Pregi, Nicolás
Wenker, Shirley Denise
Vittori, Daniela Cecilia
Perez Leiros, Claudia
Nesse, Alcira Beatriz
author_role author
author2 Wenker, Shirley Denise
Vittori, Daniela Cecilia
Perez Leiros, Claudia
Nesse, Alcira Beatriz
author2_role author
author
author
author
dc.subject.none.fl_str_mv Apoptosis
Erythropoietin
Inflammation
Neuroprotection
Nf-ΚB
Sh-Sy5y Cells
Tnf-Α
topic Apoptosis
Erythropoietin
Inflammation
Neuroprotection
Nf-ΚB
Sh-Sy5y Cells
Tnf-Α
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv The growth factor erythropoietin (Epo) has shown neuronal protective action in addition to its well known proerythroid activity. Furthermore, Epo has dealt with cellular inflammation by inhibiting the expression of several proinflammatory cytokines, such as IL-1 and TNF-α. The action of TNF can have both apoptotic and antiapoptotic consequences due to altered balance between different cell signalling pathways. This work has focused on the apoptotic effects of this cytokine and the potential protective action of Epo. The model we used was neuroblastoma SH-SY5Y cells cultured in the presence of 25 ng/ml TNF-α or pretreated with 25 U/ml Epo for 12 h before the addition of TNF-α. Apoptosis was evaluated by differential cell count after Hoechst staining, analysis of DNA ladder pattern, and measurement of caspase activity. Despite its ability to induce NF-κB nuclear translocation, TNF-α induced cell death, which was found to be associated to upregulation of TNF Receptor 1 expression. On the other hand, cells activated by Epo became resistant to cell death. Prevention of death receptor upregulation and caspase activation may explain this antiapoptotic effect of Epo, which may be also favoured by the induction of a higher expression of protective factors, such as Bcl-2 and NF-κB, through mechanisms involving Jak/STAT and PI3K signalling pathways. © 2008 Elsevier Inc. All rights reserved.
Fil: Pregi, Nicolás. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; Argentina
Fil: Wenker, Shirley Denise. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; Argentina
Fil: Vittori, Daniela Cecilia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; Argentina
Fil: Perez Leiros, Claudia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; Argentina
Fil: Nesse, Alcira Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; Argentina
description The growth factor erythropoietin (Epo) has shown neuronal protective action in addition to its well known proerythroid activity. Furthermore, Epo has dealt with cellular inflammation by inhibiting the expression of several proinflammatory cytokines, such as IL-1 and TNF-α. The action of TNF can have both apoptotic and antiapoptotic consequences due to altered balance between different cell signalling pathways. This work has focused on the apoptotic effects of this cytokine and the potential protective action of Epo. The model we used was neuroblastoma SH-SY5Y cells cultured in the presence of 25 ng/ml TNF-α or pretreated with 25 U/ml Epo for 12 h before the addition of TNF-α. Apoptosis was evaluated by differential cell count after Hoechst staining, analysis of DNA ladder pattern, and measurement of caspase activity. Despite its ability to induce NF-κB nuclear translocation, TNF-α induced cell death, which was found to be associated to upregulation of TNF Receptor 1 expression. On the other hand, cells activated by Epo became resistant to cell death. Prevention of death receptor upregulation and caspase activation may explain this antiapoptotic effect of Epo, which may be also favoured by the induction of a higher expression of protective factors, such as Bcl-2 and NF-κB, through mechanisms involving Jak/STAT and PI3K signalling pathways. © 2008 Elsevier Inc. All rights reserved.
publishDate 2009
dc.date.none.fl_str_mv 2009-02
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/66372
Pregi, Nicolás; Wenker, Shirley Denise; Vittori, Daniela Cecilia; Perez Leiros, Claudia; Nesse, Alcira Beatriz; TNF-alpha-induced apoptosis is prevented by erythropoietin treatment on SH-SY5Y cells; Elsevier Inc; Experimental Cell Research; 315; 3; 2-2009; 419-431
0014-4827
CONICET Digital
CONICET
url http://hdl.handle.net/11336/66372
identifier_str_mv Pregi, Nicolás; Wenker, Shirley Denise; Vittori, Daniela Cecilia; Perez Leiros, Claudia; Nesse, Alcira Beatriz; TNF-alpha-induced apoptosis is prevented by erythropoietin treatment on SH-SY5Y cells; Elsevier Inc; Experimental Cell Research; 315; 3; 2-2009; 419-431
0014-4827
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/http://www.sciencedirect.com/science/article/pii/S0014482708004692
info:eu-repo/semantics/altIdentifier/doi/10.1016/j.yexcr.2008.11.005
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Elsevier Inc
publisher.none.fl_str_mv Elsevier Inc
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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