Utilize este identificador para referenciar este registo:
https://hdl.handle.net/10316/12763
Campo DC | Valor | Idioma |
---|---|---|
dc.contributor.author | Castro-Caldas, M. | - |
dc.contributor.author | Mendes, A. F. | - |
dc.contributor.author | Carvalho, A. P. | - |
dc.contributor.author | Duarte, C. B. | - |
dc.contributor.author | Lopes, M. C. | - |
dc.date.accessioned | 2010-03-09T08:43:43Z | - |
dc.date.available | 2010-03-09T08:43:43Z | - |
dc.date.issued | 2003-02 | - |
dc.identifier.citation | Mediators of Inflammation. 12:1 (2003) 37-46 | en_US |
dc.identifier.issn | 0962-9351 | - |
dc.identifier.uri | https://hdl.handle.net/10316/12763 | - |
dc.description.abstract | AIMS: Glucocorticoids (GCs) exert some of their anti-inflammatory actions by preventing the activation of the transcription factor nuclear factor (NF)-kappaB. The GC-dependent inhibition of NF-kappaB may occur at different levels, but the mechanisms involved are still incompletely understood. In this work, we investigated whether the synthetic GC, dexamethasone (Dex), modulates the activity of NF-kappaB in the lymphoblastic CCRF-CEM cell line. We also evaluated the ability of Dex to prevent the activation of NF-kappaB in response to the potent proinflammatory cytokine, interleukin (IL)-1beta. RESULTS: Exposure of the cells to Dex (1 microM) induced the rapid degradation of IkappaB-alpha, leading to the transient translocation of the NF-kappaB family members p65 and p50 from the cytoplasm to the nucleus, as evaluated by western blot. Electrophoretic mobility shift assays revealed that, in the nucleus, these NF-kappaB proteins formed protein-DNA complexes, indicating a transient activation of NF-kappaB. Additionally, Dex also induced de novo synthesis of IkappaB-alpha, following its degradation. Finally, when the cells were exposed to Dex (1 microM) prior to stimulation with IL-1beta (20 ng/ml), Dex was efficient in preventing IL-1beta-induced NF-kappaB activation. The GC antagonist, RU 486 (10 microM), did not prevent any of the effects of Dex reported here. CONCLUSION: Our results indicate that, in CCRF-CEM cells, Dex prevents NF-kappaB activation, induced by IL-1beta, by a mechanism that involves the upregulation of IkappaB-alpha synthesis, and that depends on the early and transient activation of NF-kappaB | en_US |
dc.language.iso | eng | en_US |
dc.publisher | Taylor & Francis Ltd | en_US |
dc.rights | openAccess | en_US |
dc.subject | Nuclear factor-kB | en_US |
dc.subject | Dexamethasone | en_US |
dc.subject | IkB-a | en_US |
dc.subject | Interleukin-1b | en_US |
dc.subject | Lymphoblastic cells | en_US |
dc.title | Dexamethasone prevents interleukin-1beta-induced nuclear factor-kappaB activation by upregulating IkappaB-alpha synthesis, in lymphoblastic cells | en_US |
dc.type | article | en_US |
dc.identifier.doi | 10.1080/0962935031000096953 | - |
uc.controloAutoridade | Sim | - |
item.languageiso639-1 | en | - |
item.grantfulltext | open | - |
item.fulltext | Com Texto completo | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.openairetype | article | - |
item.cerifentitytype | Publications | - |
crisitem.author.researchunit | CNC - Center for Neuroscience and Cell Biology | - |
crisitem.author.researchunit | CNC - Center for Neuroscience and Cell Biology | - |
crisitem.author.orcid | 0000-0001-5511-7132 | - |
crisitem.author.orcid | 0000-0002-1474-0208 | - |
Aparece nas coleções: | FFUC- Artigos em Revistas Internacionais FCTUC Ciências da Vida - Artigos em Revistas Internacionais |
Ficheiros deste registo:
Ficheiro | Descrição | Tamanho | Formato | |
---|---|---|---|---|
Dexamethasone prevents interleukin-1beta-induced.pdf | 487.24 kB | Adobe PDF | Ver/Abrir |
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