Critical protective role for annexin 1 gene expression in the endotoxemic murine microcirculation

Detalhes bibliográficos
Autor(a) principal: Damazo, Amilcar Sabino [UNIFESP]
Data de Publicação: 2005
Outros Autores: Yona, Simon, D'Acquisto, Fulvio, Flower, Roderick J., Oliani, Sonia M. [UNIFESP], Perretti, Mauro
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNIFESP
Texto Completo: http://dx.doi.org/10.1016/S0002-9440(10)62471-6
http://repositorio.unifesp.br/handle/11600/28311
Resumo: The inflammatory response is a protective process of the body to counteract xenobiotic penetration and injury, although in disease this response can become deregulated. There are endogenous biochemical pathways that operate in the host to keep inflammation under control. Here we demonstrate that the counter-regulator annexin 1 (AnxA1) is critical for controlling experimental endotoxemia. Lipopolysaccharide (LPS) markedly activated the AnxA1 gene in epithelial cells, neutrophils, and peritoneal, mesenteric, and alveolar macrophages cell types known to function in experimental endotoxemia. Administration of LPS to AnxA1-deficient mice produced a toxic response characterized by organ injury and lethality within 48 hours, a phenotype rescued by exogenous application of low doses of the protein. in the absence of AnxA1, LPS generated a deregulated cellular and cytokine response with a marked degree of leukocyte adhesion in the microcirculation. Analysis of LPS receptor expression in AnxA1-null macrophages indicated an aberrant expression of Toll-like receptor 4. in conclusion, this study has detailed cellular and biochemical alterations associated with AnxA1 gene deletion and highlighted the impact of this protective circuit for the correct functioning of the homeostatic response to sublethal doses of LPS.
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spelling Critical protective role for annexin 1 gene expression in the endotoxemic murine microcirculationThe inflammatory response is a protective process of the body to counteract xenobiotic penetration and injury, although in disease this response can become deregulated. There are endogenous biochemical pathways that operate in the host to keep inflammation under control. Here we demonstrate that the counter-regulator annexin 1 (AnxA1) is critical for controlling experimental endotoxemia. Lipopolysaccharide (LPS) markedly activated the AnxA1 gene in epithelial cells, neutrophils, and peritoneal, mesenteric, and alveolar macrophages cell types known to function in experimental endotoxemia. Administration of LPS to AnxA1-deficient mice produced a toxic response characterized by organ injury and lethality within 48 hours, a phenotype rescued by exogenous application of low doses of the protein. in the absence of AnxA1, LPS generated a deregulated cellular and cytokine response with a marked degree of leukocyte adhesion in the microcirculation. Analysis of LPS receptor expression in AnxA1-null macrophages indicated an aberrant expression of Toll-like receptor 4. in conclusion, this study has detailed cellular and biochemical alterations associated with AnxA1 gene deletion and highlighted the impact of this protective circuit for the correct functioning of the homeostatic response to sublethal doses of LPS.Queen Mary Sch Med & Dent, Ctr Biochem Pharmacol, William Harvey Res Inst, London EC1M 6BQ, EnglandUniversidade Federal de São Paulo, Post Grad Morphol, São Paulo, BrazilUniv Estado São Paulo, Dept Biol, Inst Biociencias Letras & Ciencias Exatas, Sao Jose Do Rio Preto, SP, BrazilUniversidade Federal de São Paulo, Post Grad Morphol, São Paulo, BrazilWeb of ScienceAmer Soc Investigative Pathology, IncQueen Mary Sch Med & DentUniversidade Federal de São Paulo (UNIFESP)Univ Estado São PauloDamazo, Amilcar Sabino [UNIFESP]Yona, SimonD'Acquisto, FulvioFlower, Roderick J.Oliani, Sonia M. [UNIFESP]Perretti, Mauro2016-01-24T12:37:52Z2016-01-24T12:37:52Z2005-06-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersion1607-1617http://dx.doi.org/10.1016/S0002-9440(10)62471-6American Journal of Pathology. Bethesda: Amer Soc Investigative Pathology, Inc, v. 166, n. 6, p. 1607-1617, 2005.10.1016/S0002-9440(10)62471-60002-9440http://repositorio.unifesp.br/handle/11600/28311WOS:000229387100004engAmerican Journal of Pathologyinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP2016-03-14T14:45:34Zoai:repositorio.unifesp.br/:11600/28311Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestbiblioteca.csp@unifesp.bropendoar:34652016-03-14T14:45:34Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false
dc.title.none.fl_str_mv Critical protective role for annexin 1 gene expression in the endotoxemic murine microcirculation
title Critical protective role for annexin 1 gene expression in the endotoxemic murine microcirculation
spellingShingle Critical protective role for annexin 1 gene expression in the endotoxemic murine microcirculation
Damazo, Amilcar Sabino [UNIFESP]
title_short Critical protective role for annexin 1 gene expression in the endotoxemic murine microcirculation
title_full Critical protective role for annexin 1 gene expression in the endotoxemic murine microcirculation
title_fullStr Critical protective role for annexin 1 gene expression in the endotoxemic murine microcirculation
title_full_unstemmed Critical protective role for annexin 1 gene expression in the endotoxemic murine microcirculation
title_sort Critical protective role for annexin 1 gene expression in the endotoxemic murine microcirculation
author Damazo, Amilcar Sabino [UNIFESP]
author_facet Damazo, Amilcar Sabino [UNIFESP]
Yona, Simon
D'Acquisto, Fulvio
Flower, Roderick J.
Oliani, Sonia M. [UNIFESP]
Perretti, Mauro
author_role author
author2 Yona, Simon
D'Acquisto, Fulvio
Flower, Roderick J.
Oliani, Sonia M. [UNIFESP]
Perretti, Mauro
author2_role author
author
author
author
author
dc.contributor.none.fl_str_mv Queen Mary Sch Med & Dent
Universidade Federal de São Paulo (UNIFESP)
Univ Estado São Paulo
dc.contributor.author.fl_str_mv Damazo, Amilcar Sabino [UNIFESP]
Yona, Simon
D'Acquisto, Fulvio
Flower, Roderick J.
Oliani, Sonia M. [UNIFESP]
Perretti, Mauro
description The inflammatory response is a protective process of the body to counteract xenobiotic penetration and injury, although in disease this response can become deregulated. There are endogenous biochemical pathways that operate in the host to keep inflammation under control. Here we demonstrate that the counter-regulator annexin 1 (AnxA1) is critical for controlling experimental endotoxemia. Lipopolysaccharide (LPS) markedly activated the AnxA1 gene in epithelial cells, neutrophils, and peritoneal, mesenteric, and alveolar macrophages cell types known to function in experimental endotoxemia. Administration of LPS to AnxA1-deficient mice produced a toxic response characterized by organ injury and lethality within 48 hours, a phenotype rescued by exogenous application of low doses of the protein. in the absence of AnxA1, LPS generated a deregulated cellular and cytokine response with a marked degree of leukocyte adhesion in the microcirculation. Analysis of LPS receptor expression in AnxA1-null macrophages indicated an aberrant expression of Toll-like receptor 4. in conclusion, this study has detailed cellular and biochemical alterations associated with AnxA1 gene deletion and highlighted the impact of this protective circuit for the correct functioning of the homeostatic response to sublethal doses of LPS.
publishDate 2005
dc.date.none.fl_str_mv 2005-06-01
2016-01-24T12:37:52Z
2016-01-24T12:37:52Z
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://dx.doi.org/10.1016/S0002-9440(10)62471-6
American Journal of Pathology. Bethesda: Amer Soc Investigative Pathology, Inc, v. 166, n. 6, p. 1607-1617, 2005.
10.1016/S0002-9440(10)62471-6
0002-9440
http://repositorio.unifesp.br/handle/11600/28311
WOS:000229387100004
url http://dx.doi.org/10.1016/S0002-9440(10)62471-6
http://repositorio.unifesp.br/handle/11600/28311
identifier_str_mv American Journal of Pathology. Bethesda: Amer Soc Investigative Pathology, Inc, v. 166, n. 6, p. 1607-1617, 2005.
10.1016/S0002-9440(10)62471-6
0002-9440
WOS:000229387100004
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv American Journal of Pathology
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 1607-1617
dc.publisher.none.fl_str_mv Amer Soc Investigative Pathology, Inc
publisher.none.fl_str_mv Amer Soc Investigative Pathology, Inc
dc.source.none.fl_str_mv reponame:Repositório Institucional da UNIFESP
instname:Universidade Federal de São Paulo (UNIFESP)
instacron:UNIFESP
instname_str Universidade Federal de São Paulo (UNIFESP)
instacron_str UNIFESP
institution UNIFESP
reponame_str Repositório Institucional da UNIFESP
collection Repositório Institucional da UNIFESP
repository.name.fl_str_mv Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)
repository.mail.fl_str_mv biblioteca.csp@unifesp.br
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