Critical protective role for annexin 1 gene expression in the endotoxemic murine microcirculation
Autor(a) principal: | |
---|---|
Data de Publicação: | 2005 |
Outros Autores: | , , , , |
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. |
id |
UFSP_8b2e71aac1fed6606ccff1a1306bfcd9 |
---|---|
oai_identifier_str |
oai:repositorio.unifesp.br/:11600/28311 |
network_acronym_str |
UFSP |
network_name_str |
Repositório Institucional da UNIFESP |
repository_id_str |
3465 |
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 |
_version_ |
1814268359212007424 |