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
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/66372
Ver los metadatos del registro completo
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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 |
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CONICET Digital (CONICET) |
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CONICET Digital (CONICET) |
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Consejo Nacional de Investigaciones Científicas y Técnicas |
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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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