SOCS3 expression correlates with severity of inflammation, expression of proinflammatory cytokines, and activation of STAT3 and p38 MAPK in LPS-induced inflammation in vivo
Autor(a) principal: | |
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Data de Publicação: | 2013 |
Outros Autores: | , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNESP |
Texto Completo: | http://dx.doi.org/10.1155/2013/650812 http://hdl.handle.net/11449/76797 |
Resumo: | SOCS3 is an inducible endogenous negative regulator of JAK/STAT pathway, which is relevant in inflammatory conditions. We used a model of LPS-induced periodontal disease in rats to correlate SOCS3 expression with the inflammatory status. In vitro we used a murine macrophage cell line to assess the physical interaction between SOCS3 and STAT3 by coimmunoprecipitation. 30 ug of LPS from Escherichia coli were injected in the gingival tissues on the palatal aspect of first molars of the animals 3x/week for up to 4 weeks. Control animals were injected with the vehicle (PBS). The rats were sacrificed at 7, 15, and 30 days. Inflammation and gene expression were assessed by stereometric analysis, immunohistochemistry, RT-qPCR, and western blot. LPS injections increased inflammation, paralleled by an upregulation of SOCS3, of the proinflammatory cytokines IL-1β, IL-6, and TNF-and increased phosphorylation of STAT3 and p38 MAPK. SOCS3 expression accompanied the severity of inflammation and the expression of proinflammatory cytokines, as well as the activation status of STAT3 and p38 MAPK. LPS stimulation in a macrophage cell line in vitro induced transient STAT3 activation, which was inversely correlated with a dynamic physical interaction with SOCS3, suggesting that this may be a mechanism for SOCS3 regulatory function. © 2013 João Antônio Chaves de Souza et al. |
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SOCS3 expression correlates with severity of inflammation, expression of proinflammatory cytokines, and activation of STAT3 and p38 MAPK in LPS-induced inflammation in vivoSOCS3 is an inducible endogenous negative regulator of JAK/STAT pathway, which is relevant in inflammatory conditions. We used a model of LPS-induced periodontal disease in rats to correlate SOCS3 expression with the inflammatory status. In vitro we used a murine macrophage cell line to assess the physical interaction between SOCS3 and STAT3 by coimmunoprecipitation. 30 ug of LPS from Escherichia coli were injected in the gingival tissues on the palatal aspect of first molars of the animals 3x/week for up to 4 weeks. Control animals were injected with the vehicle (PBS). The rats were sacrificed at 7, 15, and 30 days. Inflammation and gene expression were assessed by stereometric analysis, immunohistochemistry, RT-qPCR, and western blot. LPS injections increased inflammation, paralleled by an upregulation of SOCS3, of the proinflammatory cytokines IL-1β, IL-6, and TNF-and increased phosphorylation of STAT3 and p38 MAPK. SOCS3 expression accompanied the severity of inflammation and the expression of proinflammatory cytokines, as well as the activation status of STAT3 and p38 MAPK. LPS stimulation in a macrophage cell line in vitro induced transient STAT3 activation, which was inversely correlated with a dynamic physical interaction with SOCS3, suggesting that this may be a mechanism for SOCS3 regulatory function. © 2013 João Antônio Chaves de Souza et al.Department of Diagnosis and Surgery School of Dentistry at Araraquara Universidade Estadual Paulista (UNESP), Rua Humaitá, 1680-Centro, 14801-903 Araraquara, SPDepartment of Physiology and Pathology School of Dentistry at Araraquara Universidade Estadual Paulista (UNESP), 14801-903 Araraquara, SPDepartment of Implantology University of Santo Amaro, 04743-030 Santo Amaro, SPDepartment of Biological Sciences School of Dentistry at Bauru University of São Paulo (USP), 17012-901 Bauru, SPDepartment of Diagnosis and Surgery School of Dentistry at Araraquara Universidade Estadual Paulista (UNESP), Rua Humaitá, 1680-Centro, 14801-903 Araraquara, SPDepartment of Physiology and Pathology School of Dentistry at Araraquara Universidade Estadual Paulista (UNESP), 14801-903 Araraquara, SPUniversidade Estadual Paulista (Unesp)University of Santo AmaroUniversidade de São Paulo (USP)Chaves de Souza, João Antônio [UNESP]Nogueira, Andressa Vilas Boas [UNESP]Chaves de Souza, Pedro Paulo [UNESP]Kim, Yeon JungSilva Lobo, Caroline [UNESP]Pimentel Lopes de Oliveira, Guilherme José [UNESP]Cirelli, Joni Augusto [UNESP]Garlet, Gustavo PompermaierRossa, Carlos [UNESP]2014-05-27T11:30:50Z2014-05-27T11:30:50Z2013-10-07info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleapplication/pdfhttp://dx.doi.org/10.1155/2013/650812Mediators of Inflammation, v. 2013.0962-93511466-1861http://hdl.handle.net/11449/7679710.1155/2013/650812WOS:0003244260000012-s2.0-848848887232-s2.0-84884888723.pdf2628593693450121Scopusreponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengMediators of Inflammation3.5491,3701,370info:eu-repo/semantics/openAccess2024-01-27T06:54:37Zoai:repositorio.unesp.br:11449/76797Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462024-08-06T00:04:25.134017Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false |
dc.title.none.fl_str_mv |
SOCS3 expression correlates with severity of inflammation, expression of proinflammatory cytokines, and activation of STAT3 and p38 MAPK in LPS-induced inflammation in vivo |
title |
SOCS3 expression correlates with severity of inflammation, expression of proinflammatory cytokines, and activation of STAT3 and p38 MAPK in LPS-induced inflammation in vivo |
spellingShingle |
SOCS3 expression correlates with severity of inflammation, expression of proinflammatory cytokines, and activation of STAT3 and p38 MAPK in LPS-induced inflammation in vivo Chaves de Souza, João Antônio [UNESP] |
title_short |
SOCS3 expression correlates with severity of inflammation, expression of proinflammatory cytokines, and activation of STAT3 and p38 MAPK in LPS-induced inflammation in vivo |
title_full |
SOCS3 expression correlates with severity of inflammation, expression of proinflammatory cytokines, and activation of STAT3 and p38 MAPK in LPS-induced inflammation in vivo |
title_fullStr |
SOCS3 expression correlates with severity of inflammation, expression of proinflammatory cytokines, and activation of STAT3 and p38 MAPK in LPS-induced inflammation in vivo |
title_full_unstemmed |
SOCS3 expression correlates with severity of inflammation, expression of proinflammatory cytokines, and activation of STAT3 and p38 MAPK in LPS-induced inflammation in vivo |
title_sort |
SOCS3 expression correlates with severity of inflammation, expression of proinflammatory cytokines, and activation of STAT3 and p38 MAPK in LPS-induced inflammation in vivo |
author |
Chaves de Souza, João Antônio [UNESP] |
author_facet |
Chaves de Souza, João Antônio [UNESP] Nogueira, Andressa Vilas Boas [UNESP] Chaves de Souza, Pedro Paulo [UNESP] Kim, Yeon Jung Silva Lobo, Caroline [UNESP] Pimentel Lopes de Oliveira, Guilherme José [UNESP] Cirelli, Joni Augusto [UNESP] Garlet, Gustavo Pompermaier Rossa, Carlos [UNESP] |
author_role |
author |
author2 |
Nogueira, Andressa Vilas Boas [UNESP] Chaves de Souza, Pedro Paulo [UNESP] Kim, Yeon Jung Silva Lobo, Caroline [UNESP] Pimentel Lopes de Oliveira, Guilherme José [UNESP] Cirelli, Joni Augusto [UNESP] Garlet, Gustavo Pompermaier Rossa, Carlos [UNESP] |
author2_role |
author author author author author author author author |
dc.contributor.none.fl_str_mv |
Universidade Estadual Paulista (Unesp) University of Santo Amaro Universidade de São Paulo (USP) |
dc.contributor.author.fl_str_mv |
Chaves de Souza, João Antônio [UNESP] Nogueira, Andressa Vilas Boas [UNESP] Chaves de Souza, Pedro Paulo [UNESP] Kim, Yeon Jung Silva Lobo, Caroline [UNESP] Pimentel Lopes de Oliveira, Guilherme José [UNESP] Cirelli, Joni Augusto [UNESP] Garlet, Gustavo Pompermaier Rossa, Carlos [UNESP] |
description |
SOCS3 is an inducible endogenous negative regulator of JAK/STAT pathway, which is relevant in inflammatory conditions. We used a model of LPS-induced periodontal disease in rats to correlate SOCS3 expression with the inflammatory status. In vitro we used a murine macrophage cell line to assess the physical interaction between SOCS3 and STAT3 by coimmunoprecipitation. 30 ug of LPS from Escherichia coli were injected in the gingival tissues on the palatal aspect of first molars of the animals 3x/week for up to 4 weeks. Control animals were injected with the vehicle (PBS). The rats were sacrificed at 7, 15, and 30 days. Inflammation and gene expression were assessed by stereometric analysis, immunohistochemistry, RT-qPCR, and western blot. LPS injections increased inflammation, paralleled by an upregulation of SOCS3, of the proinflammatory cytokines IL-1β, IL-6, and TNF-and increased phosphorylation of STAT3 and p38 MAPK. SOCS3 expression accompanied the severity of inflammation and the expression of proinflammatory cytokines, as well as the activation status of STAT3 and p38 MAPK. LPS stimulation in a macrophage cell line in vitro induced transient STAT3 activation, which was inversely correlated with a dynamic physical interaction with SOCS3, suggesting that this may be a mechanism for SOCS3 regulatory function. © 2013 João Antônio Chaves de Souza et al. |
publishDate |
2013 |
dc.date.none.fl_str_mv |
2013-10-07 2014-05-27T11:30:50Z 2014-05-27T11:30:50Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://dx.doi.org/10.1155/2013/650812 Mediators of Inflammation, v. 2013. 0962-9351 1466-1861 http://hdl.handle.net/11449/76797 10.1155/2013/650812 WOS:000324426000001 2-s2.0-84884888723 2-s2.0-84884888723.pdf 2628593693450121 |
url |
http://dx.doi.org/10.1155/2013/650812 http://hdl.handle.net/11449/76797 |
identifier_str_mv |
Mediators of Inflammation, v. 2013. 0962-9351 1466-1861 10.1155/2013/650812 WOS:000324426000001 2-s2.0-84884888723 2-s2.0-84884888723.pdf 2628593693450121 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Mediators of Inflammation 3.549 1,370 1,370 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
application/pdf |
dc.source.none.fl_str_mv |
Scopus reponame:Repositório Institucional da UNESP instname:Universidade Estadual Paulista (UNESP) instacron:UNESP |
instname_str |
Universidade Estadual Paulista (UNESP) |
instacron_str |
UNESP |
institution |
UNESP |
reponame_str |
Repositório Institucional da UNESP |
collection |
Repositório Institucional da UNESP |
repository.name.fl_str_mv |
Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP) |
repository.mail.fl_str_mv |
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1808129579932450816 |