التفاصيل البيبلوغرافية
| العنوان: |
TNF-alpha-induced apoptosis is prevented by erythropoietin treatment on SH-SY5Y cells |
| المؤلفون: |
Pregi, Nicolás, Wenker, Shirley Denise, Vittori, Daniela Cecilia, Pérez Leirós, Claudia, Nesse, Alcira Beatriz |
| سنة النشر: |
2009 |
| المجموعة: |
Biblioteca Digital FCEN-UBA (Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires) |
| مصطلحات موضوعية: |
Apoptosis, Erythropoietin, Inflammation, Neuroprotection, NF-κB, SH-SY5Y cells, TNF-α, caspase, Janus kinase, phosphatidylinositol 3 kinase, STAT protein, tumor necrosis factor alpha, tumor necrosis factor receptor 1, article, cell death, cell line, controlled study, enzyme activation, enzyme activity, human, human cell, priority journal, protein transport |
| الوصف: |
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, N. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. ; Fil:Wenker, S. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. ; Fil:Vittori, D. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. ; Fil:Leirós, C.P. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. ; Fil:Nesse, A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. |
| نوع الوثيقة: |
other/unknown material |
| اللغة: |
unknown |
| Relation: |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00144827_v315_n3_p419_Pregi; http://hdl.handle.net/20.500.12110/paper_00144827_v315_n3_p419_Pregi |
| الاتاحة: |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00144827_v315_n3_p419_Pregi
https://hdl.handle.net/20.500.12110/paper_00144827_v315_n3_p419_Pregi |
| رقم الانضمام: |
edsbas.633A88CA |
| قاعدة البيانات: |
BASE |