Mechanisms underlying the modulatory action of platelet activating factor (PAF) on the upregulation of kinin B-1 receptors in the rat paw
Autor(a) principal: | |
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Data de Publicação: | 2003 |
Outros Autores: | , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNIFESP |
Texto Completo: | http://dx.doi.org/10.1038/sj.bjp.0705314 http://repositorio.unifesp.br/handle/11600/27294 |
Resumo: | 1 the present study evaluated the ability of the administration of platelet activating factor (PAF) to induce the upregulation of B-1 receptors in the rat paw.2 Local treatment with PAF resulted in a time-dependent increase of oedema formation induced by the B-1 receptor agonist des-Arg(9)-BK (des-Arg(9)-bradykinin), but not by the B-2 receptor agonist tyrosine 8-bradykinin. Functional upregulation of B-1 receptors was accompanied by a prominent increase of B-1 receptor mRNA expression in the rat paw.3 in PAF-treated paws, des-Arg(9)-BK-induced oedema formation was significantly inhibited by the B1 receptor antagonists des-Arg(9)-[Leu(8)]-BK and R-715. the effects of PAF pretreatment were receptor operated, as assessed by the effects of the PAF receptor antagonist WEB2086 or by desensitisation of PAF receptors.4 the protein synthesis inhibitor cycloheximide, the anti-inflammatory steroid dexamethasone or the nuclear factor (NF-kappaB) blockers pyrrolidine-dithiocarbamate ( PDTC) and Nalpha-tosyl-L-chloromethylketone significantly blocked the functional upregulation of B-1 receptors.5 the selectin inhibitor fucoidin, an anti-CD18 antibody or an anti-rat neutrophil antiserum, also significantly prevented des-Arg(9)-BK-induced paw oedema in rats pretreated with PAF.6 Intradermal injection of PAF induced a 25-fold increase of myeloperoxidase activity in the rat paw, a response that was significantly inhibited by fucoidin, anti-CD-18, anti-rat neutrophil antiserum or PDTC.7 Local treatment with PAF also resulted in a marked increase of NF-kappaB activation, an effect largely prevented by PDTC or by the anti-rat neutrophil antiserum.8 Collectively, the present results indicate that the induction of B-1 receptors following treatment with the chemotatic mediator PAF is dependent on the recruitment of neutrophils, an event that is under the control of adhesion molecules, protein synthesis and NF-kappaB activation. These findings provide new insights into the role played by cell migration and chemotatic factors on B-1 receptor upregulation in vivo. |
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Mechanisms underlying the modulatory action of platelet activating factor (PAF) on the upregulation of kinin B-1 receptors in the rat pawB-1 receptor expressionplatelet activating factoroedema formationneutrophil influxmyeloperoxidase activityNF-kappa B binding activation1 the present study evaluated the ability of the administration of platelet activating factor (PAF) to induce the upregulation of B-1 receptors in the rat paw.2 Local treatment with PAF resulted in a time-dependent increase of oedema formation induced by the B-1 receptor agonist des-Arg(9)-BK (des-Arg(9)-bradykinin), but not by the B-2 receptor agonist tyrosine 8-bradykinin. Functional upregulation of B-1 receptors was accompanied by a prominent increase of B-1 receptor mRNA expression in the rat paw.3 in PAF-treated paws, des-Arg(9)-BK-induced oedema formation was significantly inhibited by the B1 receptor antagonists des-Arg(9)-[Leu(8)]-BK and R-715. the effects of PAF pretreatment were receptor operated, as assessed by the effects of the PAF receptor antagonist WEB2086 or by desensitisation of PAF receptors.4 the protein synthesis inhibitor cycloheximide, the anti-inflammatory steroid dexamethasone or the nuclear factor (NF-kappaB) blockers pyrrolidine-dithiocarbamate ( PDTC) and Nalpha-tosyl-L-chloromethylketone significantly blocked the functional upregulation of B-1 receptors.5 the selectin inhibitor fucoidin, an anti-CD18 antibody or an anti-rat neutrophil antiserum, also significantly prevented des-Arg(9)-BK-induced paw oedema in rats pretreated with PAF.6 Intradermal injection of PAF induced a 25-fold increase of myeloperoxidase activity in the rat paw, a response that was significantly inhibited by fucoidin, anti-CD-18, anti-rat neutrophil antiserum or PDTC.7 Local treatment with PAF also resulted in a marked increase of NF-kappaB activation, an effect largely prevented by PDTC or by the anti-rat neutrophil antiserum.8 Collectively, the present results indicate that the induction of B-1 receptors following treatment with the chemotatic mediator PAF is dependent on the recruitment of neutrophils, an event that is under the control of adhesion molecules, protein synthesis and NF-kappaB activation. These findings provide new insights into the role played by cell migration and chemotatic factors on B-1 receptor upregulation in vivo.Univ Fed Santa Catarina, Ctr Biol Sci, Dept Pharmacol, BR-88015420 Florianopolis, SC, BrazilUniv Fed Minas Gerais, Dept Physiol & Biophys, Belo Horizonte, MG, BrazilUniversidade Federal de São Paulo, Escola Paulista Med, Dept Pharmacol, Sect Expt Endocrinol, BR-04044020 São Paulo, BrazilUniv Fed Minas Gerais, Dept Biochem & Immunol, Belo Horizonte, MG, BrazilUniversidade Federal de São Paulo, Escola Paulista Med, Dept Pharmacol, Sect Expt Endocrinol, BR-04044020 São Paulo, BrazilWeb of ScienceNature Publishing GroupUniversidade Federal de Santa Catarina (UFSC)Universidade Federal de Minas Gerais (UFMG)Universidade Federal de São Paulo (UNIFESP)Fernandes, Elizabeth S.Passos, Giselle F.Campos, Maria M.Araujo, José GVCPesquero, Jorge L.Avelllar, Maria Cristina Werneck [UNIFESP]Teixeira, Mauro M.Calixto, João B.2016-01-24T12:33:55Z2016-01-24T12:33:55Z2003-07-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersion973-981http://dx.doi.org/10.1038/sj.bjp.0705314British Journal of Pharmacology. London: Nature Publishing Group, v. 139, n. 5, p. 973-981, 2003.10.1038/sj.bjp.07053140007-1188http://repositorio.unifesp.br/handle/11600/27294WOS:000184066800013engBritish Journal of Pharmacologyinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP2016-01-24T10:33:55Zoai:repositorio.unifesp.br/:11600/27294Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestbiblioteca.csp@unifesp.bropendoar:34652016-01-24T10:33:55Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false |
dc.title.none.fl_str_mv |
Mechanisms underlying the modulatory action of platelet activating factor (PAF) on the upregulation of kinin B-1 receptors in the rat paw |
title |
Mechanisms underlying the modulatory action of platelet activating factor (PAF) on the upregulation of kinin B-1 receptors in the rat paw |
spellingShingle |
Mechanisms underlying the modulatory action of platelet activating factor (PAF) on the upregulation of kinin B-1 receptors in the rat paw Fernandes, Elizabeth S. B-1 receptor expression platelet activating factor oedema formation neutrophil influx myeloperoxidase activity NF-kappa B binding activation |
title_short |
Mechanisms underlying the modulatory action of platelet activating factor (PAF) on the upregulation of kinin B-1 receptors in the rat paw |
title_full |
Mechanisms underlying the modulatory action of platelet activating factor (PAF) on the upregulation of kinin B-1 receptors in the rat paw |
title_fullStr |
Mechanisms underlying the modulatory action of platelet activating factor (PAF) on the upregulation of kinin B-1 receptors in the rat paw |
title_full_unstemmed |
Mechanisms underlying the modulatory action of platelet activating factor (PAF) on the upregulation of kinin B-1 receptors in the rat paw |
title_sort |
Mechanisms underlying the modulatory action of platelet activating factor (PAF) on the upregulation of kinin B-1 receptors in the rat paw |
author |
Fernandes, Elizabeth S. |
author_facet |
Fernandes, Elizabeth S. Passos, Giselle F. Campos, Maria M. Araujo, José GVC Pesquero, Jorge L. Avelllar, Maria Cristina Werneck [UNIFESP] Teixeira, Mauro M. Calixto, João B. |
author_role |
author |
author2 |
Passos, Giselle F. Campos, Maria M. Araujo, José GVC Pesquero, Jorge L. Avelllar, Maria Cristina Werneck [UNIFESP] Teixeira, Mauro M. Calixto, João B. |
author2_role |
author author author author author author author |
dc.contributor.none.fl_str_mv |
Universidade Federal de Santa Catarina (UFSC) Universidade Federal de Minas Gerais (UFMG) Universidade Federal de São Paulo (UNIFESP) |
dc.contributor.author.fl_str_mv |
Fernandes, Elizabeth S. Passos, Giselle F. Campos, Maria M. Araujo, José GVC Pesquero, Jorge L. Avelllar, Maria Cristina Werneck [UNIFESP] Teixeira, Mauro M. Calixto, João B. |
dc.subject.por.fl_str_mv |
B-1 receptor expression platelet activating factor oedema formation neutrophil influx myeloperoxidase activity NF-kappa B binding activation |
topic |
B-1 receptor expression platelet activating factor oedema formation neutrophil influx myeloperoxidase activity NF-kappa B binding activation |
description |
1 the present study evaluated the ability of the administration of platelet activating factor (PAF) to induce the upregulation of B-1 receptors in the rat paw.2 Local treatment with PAF resulted in a time-dependent increase of oedema formation induced by the B-1 receptor agonist des-Arg(9)-BK (des-Arg(9)-bradykinin), but not by the B-2 receptor agonist tyrosine 8-bradykinin. Functional upregulation of B-1 receptors was accompanied by a prominent increase of B-1 receptor mRNA expression in the rat paw.3 in PAF-treated paws, des-Arg(9)-BK-induced oedema formation was significantly inhibited by the B1 receptor antagonists des-Arg(9)-[Leu(8)]-BK and R-715. the effects of PAF pretreatment were receptor operated, as assessed by the effects of the PAF receptor antagonist WEB2086 or by desensitisation of PAF receptors.4 the protein synthesis inhibitor cycloheximide, the anti-inflammatory steroid dexamethasone or the nuclear factor (NF-kappaB) blockers pyrrolidine-dithiocarbamate ( PDTC) and Nalpha-tosyl-L-chloromethylketone significantly blocked the functional upregulation of B-1 receptors.5 the selectin inhibitor fucoidin, an anti-CD18 antibody or an anti-rat neutrophil antiserum, also significantly prevented des-Arg(9)-BK-induced paw oedema in rats pretreated with PAF.6 Intradermal injection of PAF induced a 25-fold increase of myeloperoxidase activity in the rat paw, a response that was significantly inhibited by fucoidin, anti-CD-18, anti-rat neutrophil antiserum or PDTC.7 Local treatment with PAF also resulted in a marked increase of NF-kappaB activation, an effect largely prevented by PDTC or by the anti-rat neutrophil antiserum.8 Collectively, the present results indicate that the induction of B-1 receptors following treatment with the chemotatic mediator PAF is dependent on the recruitment of neutrophils, an event that is under the control of adhesion molecules, protein synthesis and NF-kappaB activation. These findings provide new insights into the role played by cell migration and chemotatic factors on B-1 receptor upregulation in vivo. |
publishDate |
2003 |
dc.date.none.fl_str_mv |
2003-07-01 2016-01-24T12:33:55Z 2016-01-24T12:33:55Z |
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/10.1038/sj.bjp.0705314 British Journal of Pharmacology. London: Nature Publishing Group, v. 139, n. 5, p. 973-981, 2003. 10.1038/sj.bjp.0705314 0007-1188 http://repositorio.unifesp.br/handle/11600/27294 WOS:000184066800013 |
url |
http://dx.doi.org/10.1038/sj.bjp.0705314 http://repositorio.unifesp.br/handle/11600/27294 |
identifier_str_mv |
British Journal of Pharmacology. London: Nature Publishing Group, v. 139, n. 5, p. 973-981, 2003. 10.1038/sj.bjp.0705314 0007-1188 WOS:000184066800013 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
British Journal of Pharmacology |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
973-981 |
dc.publisher.none.fl_str_mv |
Nature Publishing Group |
publisher.none.fl_str_mv |
Nature Publishing Group |
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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1814268363889704960 |