ACE2-angiotensin-(1-7)-Mas axis in renal ischaemia/reperfusion injury in rats

Detalhes bibliográficos
Autor(a) principal: Silveira, Katia D. da
Data de Publicação: 2010
Outros Autores: Bosco, Kenia S. Pompermayer, Diniz, Lucio R. L., Carmona, Adriana Karaoglanovic [UNIFESP], Cassali, Giovanni D., Bruna-Romero, Oscar, Sousa, Lirlandia P. de, Teixeira, Mauro M., Santos, Robson A. S., Simoes e Silva, Ana C., Ribeiro Vieira, Maria A.
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNIFESP
Texto Completo: http://dx.doi.org/10.1042/CS20090554
http://repositorio.unifesp.br/handle/11600/33007
Resumo: AngII (angiotensin II), ACE (angiotensin I-converting enzyme) and the AT(1) receptor (AngII type I receptor) are associated with the inflammatory process and microvascular dysfunction of AKI (acute kidney injury) induced by renal I/R (ischaemia/reperfusion). However, Ang-(1-7) [angiotensin-(1-7)], ACE2 (angiotensin I-converting enzyme 2) and the Mas receptor also play a role in renal disease models. Therefore, in the present study, we have examined the renal profile of Ang-(1-7), ACE2 and the Mas receptor in renal I/R and compared them with that of AngII, ACE and the AT(1) receptor. Male Wistar rats were submitted to left nephrectomy and ischaemia (45 min) followed by reperfusion (2 or 4 h) in the right kidney. At 4 h of reperfusion, renal AngII was increased (P < 0.01) and renal Ang-(1-7) was decreased substantially (P < 0.05), although plasma levels of both angiotensins were unchanged. in addition, renal I/R decreased the renal mRNA expression of renin (P < 0.05), AT(1) receptors (P < 0.001) and ACE2 (P < 0.05). At 2 and 4 h of reperfusion, renal ACE activity was reduced (P < 0.05). On the other hand, renal expression of the Mas receptor was greatly increased at 4 h of reperfusion (P < 0.01), which was confirmed by immunohistochemical and Western blot analysis. in conclusion, increased renal expression of the Mas receptor associated with changes in the RAS (renin-angiotensin-system)-related peptidases support an important role for the ACE2 Ang-(1-7) Mas axis in AKI.
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spelling ACE2-angiotensin-(1-7)-Mas axis in renal ischaemia/reperfusion injury in ratsacute kidney injuryangiotensin I-converting enzyme (ACE)angiotensin I-converting enzyme 2 (ACE2)angiotensin-(1-7) [Ang-(1-7)]angiotensin II (AngII)Mas receptorAngII (angiotensin II), ACE (angiotensin I-converting enzyme) and the AT(1) receptor (AngII type I receptor) are associated with the inflammatory process and microvascular dysfunction of AKI (acute kidney injury) induced by renal I/R (ischaemia/reperfusion). However, Ang-(1-7) [angiotensin-(1-7)], ACE2 (angiotensin I-converting enzyme 2) and the Mas receptor also play a role in renal disease models. Therefore, in the present study, we have examined the renal profile of Ang-(1-7), ACE2 and the Mas receptor in renal I/R and compared them with that of AngII, ACE and the AT(1) receptor. Male Wistar rats were submitted to left nephrectomy and ischaemia (45 min) followed by reperfusion (2 or 4 h) in the right kidney. At 4 h of reperfusion, renal AngII was increased (P < 0.01) and renal Ang-(1-7) was decreased substantially (P < 0.05), although plasma levels of both angiotensins were unchanged. in addition, renal I/R decreased the renal mRNA expression of renin (P < 0.05), AT(1) receptors (P < 0.001) and ACE2 (P < 0.05). At 2 and 4 h of reperfusion, renal ACE activity was reduced (P < 0.05). On the other hand, renal expression of the Mas receptor was greatly increased at 4 h of reperfusion (P < 0.01), which was confirmed by immunohistochemical and Western blot analysis. in conclusion, increased renal expression of the Mas receptor associated with changes in the RAS (renin-angiotensin-system)-related peptidases support an important role for the ACE2 Ang-(1-7) Mas axis in AKI.Univ Fed Minas Gerais, Inst Biol Sci, Dept Physiol & Biophys, BR-31270901 Belo Horizonte, MG, BrazilUniversidade Federal de São Paulo, Escola Paulista Med, Dept Biophys, BR-04044020 São Paulo, SP, BrazilUniv Fed Minas Gerais, Dept Pathol, BR-31270901 Belo Horizonte, MG, BrazilUniv Fed Minas Gerais, Dept Microbiol, BR-31270901 Belo Horizonte, MG, BrazilUniv Fed Minas Gerais, Clin Pathol Unit COLTEC, BR-31270901 Belo Horizonte, MG, BrazilUniv Fed Minas Gerais, Dept Biochem, Inst Biol Sci, BR-31270901 Belo Horizonte, MG, BrazilUniv Fed Minas Gerais, Dept Pediat, Fac Med, BR-31270901 Belo Horizonte, MG, BrazilUniversidade Federal de São Paulo, Escola Paulista Med, Dept Biophys, BR-04044020 São Paulo, SP, BrazilWeb of ScienceCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Fundação de Amparo à Pesquisa do Estado de Minas Gerais (FAPEMIG)CAPES: PRDEX2009CNPq: 8701480/1997-4FAPEMIG: CBS 2044/96Portland Press LtdUniversidade Federal de Minas Gerais (UFMG)Universidade Federal de São Paulo (UNIFESP)Silveira, Katia D. daBosco, Kenia S. PompermayerDiniz, Lucio R. L.Carmona, Adriana Karaoglanovic [UNIFESP]Cassali, Giovanni D.Bruna-Romero, OscarSousa, Lirlandia P. deTeixeira, Mauro M.Santos, Robson A. S.Simoes e Silva, Ana C.Ribeiro Vieira, Maria A.2016-01-24T14:05:35Z2016-01-24T14:05:35Z2010-11-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersion385-394http://dx.doi.org/10.1042/CS20090554Clinical Science. London: Portland Press Ltd, v. 119, n. 9-10, p. 385-394, 2010.10.1042/CS200905540143-5221http://repositorio.unifesp.br/handle/11600/33007WOS:000284130000003engClinical Scienceinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP2022-06-02T09:34:41Zoai:repositorio.unifesp.br/:11600/33007Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestbiblioteca.csp@unifesp.bropendoar:34652022-06-02T09:34:41Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false
dc.title.none.fl_str_mv ACE2-angiotensin-(1-7)-Mas axis in renal ischaemia/reperfusion injury in rats
title ACE2-angiotensin-(1-7)-Mas axis in renal ischaemia/reperfusion injury in rats
spellingShingle ACE2-angiotensin-(1-7)-Mas axis in renal ischaemia/reperfusion injury in rats
Silveira, Katia D. da
acute kidney injury
angiotensin I-converting enzyme (ACE)
angiotensin I-converting enzyme 2 (ACE2)
angiotensin-(1-7) [Ang-(1-7)]
angiotensin II (AngII)
Mas receptor
title_short ACE2-angiotensin-(1-7)-Mas axis in renal ischaemia/reperfusion injury in rats
title_full ACE2-angiotensin-(1-7)-Mas axis in renal ischaemia/reperfusion injury in rats
title_fullStr ACE2-angiotensin-(1-7)-Mas axis in renal ischaemia/reperfusion injury in rats
title_full_unstemmed ACE2-angiotensin-(1-7)-Mas axis in renal ischaemia/reperfusion injury in rats
title_sort ACE2-angiotensin-(1-7)-Mas axis in renal ischaemia/reperfusion injury in rats
author Silveira, Katia D. da
author_facet Silveira, Katia D. da
Bosco, Kenia S. Pompermayer
Diniz, Lucio R. L.
Carmona, Adriana Karaoglanovic [UNIFESP]
Cassali, Giovanni D.
Bruna-Romero, Oscar
Sousa, Lirlandia P. de
Teixeira, Mauro M.
Santos, Robson A. S.
Simoes e Silva, Ana C.
Ribeiro Vieira, Maria A.
author_role author
author2 Bosco, Kenia S. Pompermayer
Diniz, Lucio R. L.
Carmona, Adriana Karaoglanovic [UNIFESP]
Cassali, Giovanni D.
Bruna-Romero, Oscar
Sousa, Lirlandia P. de
Teixeira, Mauro M.
Santos, Robson A. S.
Simoes e Silva, Ana C.
Ribeiro Vieira, Maria A.
author2_role author
author
author
author
author
author
author
author
author
author
dc.contributor.none.fl_str_mv Universidade Federal de Minas Gerais (UFMG)
Universidade Federal de São Paulo (UNIFESP)
dc.contributor.author.fl_str_mv Silveira, Katia D. da
Bosco, Kenia S. Pompermayer
Diniz, Lucio R. L.
Carmona, Adriana Karaoglanovic [UNIFESP]
Cassali, Giovanni D.
Bruna-Romero, Oscar
Sousa, Lirlandia P. de
Teixeira, Mauro M.
Santos, Robson A. S.
Simoes e Silva, Ana C.
Ribeiro Vieira, Maria A.
dc.subject.por.fl_str_mv acute kidney injury
angiotensin I-converting enzyme (ACE)
angiotensin I-converting enzyme 2 (ACE2)
angiotensin-(1-7) [Ang-(1-7)]
angiotensin II (AngII)
Mas receptor
topic acute kidney injury
angiotensin I-converting enzyme (ACE)
angiotensin I-converting enzyme 2 (ACE2)
angiotensin-(1-7) [Ang-(1-7)]
angiotensin II (AngII)
Mas receptor
description AngII (angiotensin II), ACE (angiotensin I-converting enzyme) and the AT(1) receptor (AngII type I receptor) are associated with the inflammatory process and microvascular dysfunction of AKI (acute kidney injury) induced by renal I/R (ischaemia/reperfusion). However, Ang-(1-7) [angiotensin-(1-7)], ACE2 (angiotensin I-converting enzyme 2) and the Mas receptor also play a role in renal disease models. Therefore, in the present study, we have examined the renal profile of Ang-(1-7), ACE2 and the Mas receptor in renal I/R and compared them with that of AngII, ACE and the AT(1) receptor. Male Wistar rats were submitted to left nephrectomy and ischaemia (45 min) followed by reperfusion (2 or 4 h) in the right kidney. At 4 h of reperfusion, renal AngII was increased (P < 0.01) and renal Ang-(1-7) was decreased substantially (P < 0.05), although plasma levels of both angiotensins were unchanged. in addition, renal I/R decreased the renal mRNA expression of renin (P < 0.05), AT(1) receptors (P < 0.001) and ACE2 (P < 0.05). At 2 and 4 h of reperfusion, renal ACE activity was reduced (P < 0.05). On the other hand, renal expression of the Mas receptor was greatly increased at 4 h of reperfusion (P < 0.01), which was confirmed by immunohistochemical and Western blot analysis. in conclusion, increased renal expression of the Mas receptor associated with changes in the RAS (renin-angiotensin-system)-related peptidases support an important role for the ACE2 Ang-(1-7) Mas axis in AKI.
publishDate 2010
dc.date.none.fl_str_mv 2010-11-01
2016-01-24T14:05:35Z
2016-01-24T14:05:35Z
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/10.1042/CS20090554
Clinical Science. London: Portland Press Ltd, v. 119, n. 9-10, p. 385-394, 2010.
10.1042/CS20090554
0143-5221
http://repositorio.unifesp.br/handle/11600/33007
WOS:000284130000003
url http://dx.doi.org/10.1042/CS20090554
http://repositorio.unifesp.br/handle/11600/33007
identifier_str_mv Clinical Science. London: Portland Press Ltd, v. 119, n. 9-10, p. 385-394, 2010.
10.1042/CS20090554
0143-5221
WOS:000284130000003
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv Clinical Science
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 385-394
dc.publisher.none.fl_str_mv Portland Press Ltd
publisher.none.fl_str_mv Portland Press Ltd
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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