NITRIC OXIDE INTERFERES WITH HYPOXIA SIGNALING DURING COLONIC INFLAMMATION
Autor(a) principal: | |
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Data de Publicação: | 2014 |
Outros Autores: | , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Arquivos de gastroenterologia (Online) |
Texto Completo: | http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0004-28032014000400302 |
Resumo: | Context Intestinal inflammation can induce a local reduction in oxygen levels that triggers an adaptive response centered on the expression of hypoxia-inducible factors (HIFs). Nitric oxide, a well-described inflammatory mediator, may interfere with hypoxia signaling. Objectives We aimed to evaluate the role of nitric oxide in hypoxia signaling during colonic inflammation. Methods Colitis was induced by single (acute) or repeated (reactivated colitis) trinitrobenzenosulfonic acid administration in rats. In addition, one group of rats with reactivated colitis was also treated with Nw-Nitro-L-arginine methyl ester hydrochloride to block nitric oxide synthase. Colitis was assessed by macroscopic score and myeloperoxidase activity in the colon samples. Hypoxia was determined using the oxygen-dependent probe, pimonidazole. The expression of HIF-1α and HIF-induced factors (vascular endothelial growth factor - VEGF and apelin) was assessed using Western blotting. Results The single or repeated administration of trinitrobenzenosulfonic acid to rats induced colitis which was characterized by a high macroscopic score and myeloperoxidase activity. Hypoxia was observed with both protocols. During acute colitis, HIF-1α expression was not increased, but VEGF and apelin were increased. HIF-1α expression was inhibited during reactivated colitis, and VEGF and apelin were not increased. Nw-Nitro-L-arginine methyl ester hydrochloride blockade during reactivated colitis restored HIF-1α, VEGF and apelin expression. Conclusions Nitric oxide could interfere with hypoxia signaling during reactivated colitis inflammation modifying the expression of proteins regulated by HIF-1α. |
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NITRIC OXIDE INTERFERES WITH HYPOXIA SIGNALING DURING COLONIC INFLAMMATIONColitisHypoxia-inducible factor 1Nitric oxideNG-Nitroarginine methyl esterEndothelial growth factors Context Intestinal inflammation can induce a local reduction in oxygen levels that triggers an adaptive response centered on the expression of hypoxia-inducible factors (HIFs). Nitric oxide, a well-described inflammatory mediator, may interfere with hypoxia signaling. Objectives We aimed to evaluate the role of nitric oxide in hypoxia signaling during colonic inflammation. Methods Colitis was induced by single (acute) or repeated (reactivated colitis) trinitrobenzenosulfonic acid administration in rats. In addition, one group of rats with reactivated colitis was also treated with Nw-Nitro-L-arginine methyl ester hydrochloride to block nitric oxide synthase. Colitis was assessed by macroscopic score and myeloperoxidase activity in the colon samples. Hypoxia was determined using the oxygen-dependent probe, pimonidazole. The expression of HIF-1α and HIF-induced factors (vascular endothelial growth factor - VEGF and apelin) was assessed using Western blotting. Results The single or repeated administration of trinitrobenzenosulfonic acid to rats induced colitis which was characterized by a high macroscopic score and myeloperoxidase activity. Hypoxia was observed with both protocols. During acute colitis, HIF-1α expression was not increased, but VEGF and apelin were increased. HIF-1α expression was inhibited during reactivated colitis, and VEGF and apelin were not increased. Nw-Nitro-L-arginine methyl ester hydrochloride blockade during reactivated colitis restored HIF-1α, VEGF and apelin expression. Conclusions Nitric oxide could interfere with hypoxia signaling during reactivated colitis inflammation modifying the expression of proteins regulated by HIF-1α. Instituto Brasileiro de Estudos e Pesquisas de Gastroenterologia e Outras Especialidades - IBEPEGE. 2014-12-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0004-28032014000400302Arquivos de Gastroenterologia v.51 n.4 2014reponame:Arquivos de gastroenterologia (Online)instname:Instituto Brasileiro de Estudos e Pesquisas de Gastroenterologiainstacron:IBEPEGE10.1590/S0004-28032014000400007info:eu-repo/semantics/openAccessCARIA,Cintia Rabelo e PaivaMOSCATO,Camila HenriqueTOMÉ,Renata Bortolin GuerraPEDRAZZOLI Jr,JoséRIBEIRO,Marcelo LimaGAMBERO,Alessandraeng2015-01-09T00:00:00Zoai:scielo:S0004-28032014000400302Revistahttp://www.scielo.br/aghttps://old.scielo.br/oai/scielo-oai.php||secretariaarqgastr@hospitaligesp.com.br1678-42190004-2803opendoar:2015-01-09T00:00Arquivos de gastroenterologia (Online) - Instituto Brasileiro de Estudos e Pesquisas de Gastroenterologiafalse |
dc.title.none.fl_str_mv |
NITRIC OXIDE INTERFERES WITH HYPOXIA SIGNALING DURING COLONIC INFLAMMATION |
title |
NITRIC OXIDE INTERFERES WITH HYPOXIA SIGNALING DURING COLONIC INFLAMMATION |
spellingShingle |
NITRIC OXIDE INTERFERES WITH HYPOXIA SIGNALING DURING COLONIC INFLAMMATION CARIA,Cintia Rabelo e Paiva Colitis Hypoxia-inducible factor 1 Nitric oxide NG-Nitroarginine methyl ester Endothelial growth factors |
title_short |
NITRIC OXIDE INTERFERES WITH HYPOXIA SIGNALING DURING COLONIC INFLAMMATION |
title_full |
NITRIC OXIDE INTERFERES WITH HYPOXIA SIGNALING DURING COLONIC INFLAMMATION |
title_fullStr |
NITRIC OXIDE INTERFERES WITH HYPOXIA SIGNALING DURING COLONIC INFLAMMATION |
title_full_unstemmed |
NITRIC OXIDE INTERFERES WITH HYPOXIA SIGNALING DURING COLONIC INFLAMMATION |
title_sort |
NITRIC OXIDE INTERFERES WITH HYPOXIA SIGNALING DURING COLONIC INFLAMMATION |
author |
CARIA,Cintia Rabelo e Paiva |
author_facet |
CARIA,Cintia Rabelo e Paiva MOSCATO,Camila Henrique TOMÉ,Renata Bortolin Guerra PEDRAZZOLI Jr,José RIBEIRO,Marcelo Lima GAMBERO,Alessandra |
author_role |
author |
author2 |
MOSCATO,Camila Henrique TOMÉ,Renata Bortolin Guerra PEDRAZZOLI Jr,José RIBEIRO,Marcelo Lima GAMBERO,Alessandra |
author2_role |
author author author author author |
dc.contributor.author.fl_str_mv |
CARIA,Cintia Rabelo e Paiva MOSCATO,Camila Henrique TOMÉ,Renata Bortolin Guerra PEDRAZZOLI Jr,José RIBEIRO,Marcelo Lima GAMBERO,Alessandra |
dc.subject.por.fl_str_mv |
Colitis Hypoxia-inducible factor 1 Nitric oxide NG-Nitroarginine methyl ester Endothelial growth factors |
topic |
Colitis Hypoxia-inducible factor 1 Nitric oxide NG-Nitroarginine methyl ester Endothelial growth factors |
description |
Context Intestinal inflammation can induce a local reduction in oxygen levels that triggers an adaptive response centered on the expression of hypoxia-inducible factors (HIFs). Nitric oxide, a well-described inflammatory mediator, may interfere with hypoxia signaling. Objectives We aimed to evaluate the role of nitric oxide in hypoxia signaling during colonic inflammation. Methods Colitis was induced by single (acute) or repeated (reactivated colitis) trinitrobenzenosulfonic acid administration in rats. In addition, one group of rats with reactivated colitis was also treated with Nw-Nitro-L-arginine methyl ester hydrochloride to block nitric oxide synthase. Colitis was assessed by macroscopic score and myeloperoxidase activity in the colon samples. Hypoxia was determined using the oxygen-dependent probe, pimonidazole. The expression of HIF-1α and HIF-induced factors (vascular endothelial growth factor - VEGF and apelin) was assessed using Western blotting. Results The single or repeated administration of trinitrobenzenosulfonic acid to rats induced colitis which was characterized by a high macroscopic score and myeloperoxidase activity. Hypoxia was observed with both protocols. During acute colitis, HIF-1α expression was not increased, but VEGF and apelin were increased. HIF-1α expression was inhibited during reactivated colitis, and VEGF and apelin were not increased. Nw-Nitro-L-arginine methyl ester hydrochloride blockade during reactivated colitis restored HIF-1α, VEGF and apelin expression. Conclusions Nitric oxide could interfere with hypoxia signaling during reactivated colitis inflammation modifying the expression of proteins regulated by HIF-1α. |
publishDate |
2014 |
dc.date.none.fl_str_mv |
2014-12-01 |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0004-28032014000400302 |
url |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0004-28032014000400302 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
10.1590/S0004-28032014000400007 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
text/html |
dc.publisher.none.fl_str_mv |
Instituto Brasileiro de Estudos e Pesquisas de Gastroenterologia e Outras Especialidades - IBEPEGE. |
publisher.none.fl_str_mv |
Instituto Brasileiro de Estudos e Pesquisas de Gastroenterologia e Outras Especialidades - IBEPEGE. |
dc.source.none.fl_str_mv |
Arquivos de Gastroenterologia v.51 n.4 2014 reponame:Arquivos de gastroenterologia (Online) instname:Instituto Brasileiro de Estudos e Pesquisas de Gastroenterologia instacron:IBEPEGE |
instname_str |
Instituto Brasileiro de Estudos e Pesquisas de Gastroenterologia |
instacron_str |
IBEPEGE |
institution |
IBEPEGE |
reponame_str |
Arquivos de gastroenterologia (Online) |
collection |
Arquivos de gastroenterologia (Online) |
repository.name.fl_str_mv |
Arquivos de gastroenterologia (Online) - Instituto Brasileiro de Estudos e Pesquisas de Gastroenterologia |
repository.mail.fl_str_mv |
||secretariaarqgastr@hospitaligesp.com.br |
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1754193347345383424 |