The renin-angiotensin system is upregulated in the cortex and hippocampus of patients with temporal lobe epilepsy related to mesial temporal sclerosis

Detalhes bibliográficos
Autor(a) principal: Arganaraz, Gustavo Adolfo [UNIFESP]
Data de Publicação: 2008
Outros Autores: Konno, Ana Carla [UNIFESP], Perosa, Sandra Regina [UNIFESP], Santiago, Joselita Ferreira Carvalho [UNIFESP], Boim, Mirian A. [UNIFESP], Vidotti, Daniela Berguio [UNIFESP], Varella, Pedro Paulo Vasconcellos [UNIFESP], Costa, Luciana Gilbert [UNIFESP], Canzian, Mauro, Porcionatto, Marimelia Aparecida [UNIFESP], Yacubian, Elza Márcia Targas [UNIFESP], Sakamoto, Americo Ceiki [UNIFESP], Carrete, Henrique [UNIFESP], Centeno, Ricardo Silva [UNIFESP], Amado, Debora [UNIFESP], Cavalheiro, Esper Abrao [UNIFESP], Silva, Jose Antonio, Naffah-Mazzacoratti, Maria da Graca [UNIFESP]
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNIFESP
Texto Completo: http://repositorio.unifesp.br/handle/11600/30809
http://dx.doi.org/10.1111/j.1528-1167.2008.01581.x
Resumo: Purpose: As reported by several authors, angiotensin II (AngII) is a proinflammatory molecule that stimulates the release of inflammatory cytokines and activates nuclear factor kappa B (NF kappa B), being also associated with the increase of cellular oxidative stress. Its production depends on the activity of the angiotensin converting enzyme (ACE) that hydrolyzes the inactive precursor angiotensin I (AngI) into AngII. It has been suggested that AngII underlies the physiopathological mechanisms of several brain disorders such as stroke, bipolar disorder, schizophrenia, and disease. the aim of the present work was to localize and quantify AngII AT1 and AT2 receptors in the cortex and hippocampus of patients with temporal lobe epilepsy related to mesial temporal sclerosis (MTS) submitted to corticoamygdalohippocampectomy for seizure control.Method: Immunohistochemistry, Western blot, and real-time PCR techniques were employed to analyze the expression of these receptors.Results: the results showed an upregulation of AngII AT1 receptor as well as its messenger ribonucleic acid (mRNA) expression in the cortex and hippocampus of patients with MTS. in addition, an increased immunoexpression of AngII AT2 receptors was found only in the hippocampus of these patients with no changes in its mRNA levels.Discussion: These data show, for the first time, changes in components of renin-angiotensin system (RAS) that could be implicated in the physiopathology of MTS.
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spelling Arganaraz, Gustavo Adolfo [UNIFESP]Konno, Ana Carla [UNIFESP]Perosa, Sandra Regina [UNIFESP]Santiago, Joselita Ferreira Carvalho [UNIFESP]Boim, Mirian A. [UNIFESP]Vidotti, Daniela Berguio [UNIFESP]Varella, Pedro Paulo Vasconcellos [UNIFESP]Costa, Luciana Gilbert [UNIFESP]Canzian, MauroPorcionatto, Marimelia Aparecida [UNIFESP]Yacubian, Elza Márcia Targas [UNIFESP]Sakamoto, Americo Ceiki [UNIFESP]Carrete, Henrique [UNIFESP]Centeno, Ricardo Silva [UNIFESP]Amado, Debora [UNIFESP]Cavalheiro, Esper Abrao [UNIFESP]Silva, Jose AntonioNaffah-Mazzacoratti, Maria da Graca [UNIFESP]Universidade Federal de São Paulo (UNIFESP)Universidade de São Paulo (USP)Nove Julho Univ2016-01-24T13:51:34Z2016-01-24T13:51:34Z2008-08-01Epilepsia. Oxford: Blackwell Publishing, v. 49, n. 8, p. 1348-1357, 2008.0013-9580http://repositorio.unifesp.br/handle/11600/30809http://dx.doi.org/10.1111/j.1528-1167.2008.01581.x10.1111/j.1528-1167.2008.01581.xWOS:000257988300008Purpose: As reported by several authors, angiotensin II (AngII) is a proinflammatory molecule that stimulates the release of inflammatory cytokines and activates nuclear factor kappa B (NF kappa B), being also associated with the increase of cellular oxidative stress. Its production depends on the activity of the angiotensin converting enzyme (ACE) that hydrolyzes the inactive precursor angiotensin I (AngI) into AngII. It has been suggested that AngII underlies the physiopathological mechanisms of several brain disorders such as stroke, bipolar disorder, schizophrenia, and disease. the aim of the present work was to localize and quantify AngII AT1 and AT2 receptors in the cortex and hippocampus of patients with temporal lobe epilepsy related to mesial temporal sclerosis (MTS) submitted to corticoamygdalohippocampectomy for seizure control.Method: Immunohistochemistry, Western blot, and real-time PCR techniques were employed to analyze the expression of these receptors.Results: the results showed an upregulation of AngII AT1 receptor as well as its messenger ribonucleic acid (mRNA) expression in the cortex and hippocampus of patients with MTS. in addition, an increased immunoexpression of AngII AT2 receptors was found only in the hippocampus of these patients with no changes in its mRNA levels.Discussion: These data show, for the first time, changes in components of renin-angiotensin system (RAS) that could be implicated in the physiopathology of MTS.Universidade Federal de São Paulo, Dept Neurol & Neurosurgery, Discipline Expt Neurol, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Neurol & Neurosurgery, Discipline Nephrol, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Pathol, São Paulo, BrazilUniv São Paulo, Sch Med, Dept Pathol, São Paulo, BrazilUniversidade Federal de São Paulo, Discipline Clin Neurol, Dept Biochem, São Paulo, BrazilUniversidade Federal de São Paulo, Discipline Clin Neurol, Dept Neurol & Neurosurg, São Paulo, BrazilNove Julho Univ, Dept Sci Rehabil, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Neurol & Neurosurgery, Discipline Expt Neurol, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Neurol & Neurosurgery, Discipline Nephrol, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Pathol, São Paulo, BrazilUniversidade Federal de São Paulo, Discipline Clin Neurol, Dept Biochem, São Paulo, BrazilUniversidade Federal de São Paulo, Discipline Clin Neurol, Dept Neurol & Neurosurg, São Paulo, BrazilWeb of Science1348-1357engBlackwell PublishingEpilepsiaangiotensin II AT1 and AT2 receptorstemporal lobe epilepsycortexhippocampusThe renin-angiotensin system is upregulated in the cortex and hippocampus of patients with temporal lobe epilepsy related to mesial temporal sclerosisinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP11600/308092022-02-18 10:09:40.206metadata only accessoai:repositorio.unifesp.br:11600/30809Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestopendoar:34652023-05-25T12:07:26.576722Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false
dc.title.en.fl_str_mv The renin-angiotensin system is upregulated in the cortex and hippocampus of patients with temporal lobe epilepsy related to mesial temporal sclerosis
title The renin-angiotensin system is upregulated in the cortex and hippocampus of patients with temporal lobe epilepsy related to mesial temporal sclerosis
spellingShingle The renin-angiotensin system is upregulated in the cortex and hippocampus of patients with temporal lobe epilepsy related to mesial temporal sclerosis
Arganaraz, Gustavo Adolfo [UNIFESP]
angiotensin II AT1 and AT2 receptors
temporal lobe epilepsy
cortex
hippocampus
title_short The renin-angiotensin system is upregulated in the cortex and hippocampus of patients with temporal lobe epilepsy related to mesial temporal sclerosis
title_full The renin-angiotensin system is upregulated in the cortex and hippocampus of patients with temporal lobe epilepsy related to mesial temporal sclerosis
title_fullStr The renin-angiotensin system is upregulated in the cortex and hippocampus of patients with temporal lobe epilepsy related to mesial temporal sclerosis
title_full_unstemmed The renin-angiotensin system is upregulated in the cortex and hippocampus of patients with temporal lobe epilepsy related to mesial temporal sclerosis
title_sort The renin-angiotensin system is upregulated in the cortex and hippocampus of patients with temporal lobe epilepsy related to mesial temporal sclerosis
author Arganaraz, Gustavo Adolfo [UNIFESP]
author_facet Arganaraz, Gustavo Adolfo [UNIFESP]
Konno, Ana Carla [UNIFESP]
Perosa, Sandra Regina [UNIFESP]
Santiago, Joselita Ferreira Carvalho [UNIFESP]
Boim, Mirian A. [UNIFESP]
Vidotti, Daniela Berguio [UNIFESP]
Varella, Pedro Paulo Vasconcellos [UNIFESP]
Costa, Luciana Gilbert [UNIFESP]
Canzian, Mauro
Porcionatto, Marimelia Aparecida [UNIFESP]
Yacubian, Elza Márcia Targas [UNIFESP]
Sakamoto, Americo Ceiki [UNIFESP]
Carrete, Henrique [UNIFESP]
Centeno, Ricardo Silva [UNIFESP]
Amado, Debora [UNIFESP]
Cavalheiro, Esper Abrao [UNIFESP]
Silva, Jose Antonio
Naffah-Mazzacoratti, Maria da Graca [UNIFESP]
author_role author
author2 Konno, Ana Carla [UNIFESP]
Perosa, Sandra Regina [UNIFESP]
Santiago, Joselita Ferreira Carvalho [UNIFESP]
Boim, Mirian A. [UNIFESP]
Vidotti, Daniela Berguio [UNIFESP]
Varella, Pedro Paulo Vasconcellos [UNIFESP]
Costa, Luciana Gilbert [UNIFESP]
Canzian, Mauro
Porcionatto, Marimelia Aparecida [UNIFESP]
Yacubian, Elza Márcia Targas [UNIFESP]
Sakamoto, Americo Ceiki [UNIFESP]
Carrete, Henrique [UNIFESP]
Centeno, Ricardo Silva [UNIFESP]
Amado, Debora [UNIFESP]
Cavalheiro, Esper Abrao [UNIFESP]
Silva, Jose Antonio
Naffah-Mazzacoratti, Maria da Graca [UNIFESP]
author2_role author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
dc.contributor.institution.none.fl_str_mv Universidade Federal de São Paulo (UNIFESP)
Universidade de São Paulo (USP)
Nove Julho Univ
dc.contributor.author.fl_str_mv Arganaraz, Gustavo Adolfo [UNIFESP]
Konno, Ana Carla [UNIFESP]
Perosa, Sandra Regina [UNIFESP]
Santiago, Joselita Ferreira Carvalho [UNIFESP]
Boim, Mirian A. [UNIFESP]
Vidotti, Daniela Berguio [UNIFESP]
Varella, Pedro Paulo Vasconcellos [UNIFESP]
Costa, Luciana Gilbert [UNIFESP]
Canzian, Mauro
Porcionatto, Marimelia Aparecida [UNIFESP]
Yacubian, Elza Márcia Targas [UNIFESP]
Sakamoto, Americo Ceiki [UNIFESP]
Carrete, Henrique [UNIFESP]
Centeno, Ricardo Silva [UNIFESP]
Amado, Debora [UNIFESP]
Cavalheiro, Esper Abrao [UNIFESP]
Silva, Jose Antonio
Naffah-Mazzacoratti, Maria da Graca [UNIFESP]
dc.subject.eng.fl_str_mv angiotensin II AT1 and AT2 receptors
temporal lobe epilepsy
cortex
hippocampus
topic angiotensin II AT1 and AT2 receptors
temporal lobe epilepsy
cortex
hippocampus
description Purpose: As reported by several authors, angiotensin II (AngII) is a proinflammatory molecule that stimulates the release of inflammatory cytokines and activates nuclear factor kappa B (NF kappa B), being also associated with the increase of cellular oxidative stress. Its production depends on the activity of the angiotensin converting enzyme (ACE) that hydrolyzes the inactive precursor angiotensin I (AngI) into AngII. It has been suggested that AngII underlies the physiopathological mechanisms of several brain disorders such as stroke, bipolar disorder, schizophrenia, and disease. the aim of the present work was to localize and quantify AngII AT1 and AT2 receptors in the cortex and hippocampus of patients with temporal lobe epilepsy related to mesial temporal sclerosis (MTS) submitted to corticoamygdalohippocampectomy for seizure control.Method: Immunohistochemistry, Western blot, and real-time PCR techniques were employed to analyze the expression of these receptors.Results: the results showed an upregulation of AngII AT1 receptor as well as its messenger ribonucleic acid (mRNA) expression in the cortex and hippocampus of patients with MTS. in addition, an increased immunoexpression of AngII AT2 receptors was found only in the hippocampus of these patients with no changes in its mRNA levels.Discussion: These data show, for the first time, changes in components of renin-angiotensin system (RAS) that could be implicated in the physiopathology of MTS.
publishDate 2008
dc.date.issued.fl_str_mv 2008-08-01
dc.date.accessioned.fl_str_mv 2016-01-24T13:51:34Z
dc.date.available.fl_str_mv 2016-01-24T13:51:34Z
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.citation.fl_str_mv Epilepsia. Oxford: Blackwell Publishing, v. 49, n. 8, p. 1348-1357, 2008.
dc.identifier.uri.fl_str_mv http://repositorio.unifesp.br/handle/11600/30809
http://dx.doi.org/10.1111/j.1528-1167.2008.01581.x
dc.identifier.issn.none.fl_str_mv 0013-9580
dc.identifier.doi.none.fl_str_mv 10.1111/j.1528-1167.2008.01581.x
dc.identifier.wos.none.fl_str_mv WOS:000257988300008
identifier_str_mv Epilepsia. Oxford: Blackwell Publishing, v. 49, n. 8, p. 1348-1357, 2008.
0013-9580
10.1111/j.1528-1167.2008.01581.x
WOS:000257988300008
url http://repositorio.unifesp.br/handle/11600/30809
http://dx.doi.org/10.1111/j.1528-1167.2008.01581.x
dc.language.iso.fl_str_mv eng
language eng
dc.relation.ispartof.none.fl_str_mv Epilepsia
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 1348-1357
dc.publisher.none.fl_str_mv Blackwell Publishing
publisher.none.fl_str_mv Blackwell Publishing
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
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