Receptor Mas contribui para o desenvolvimento do remodelamento cardíaco
Autor(a) principal: | |
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Data de Publicação: | 2016 |
Tipo de documento: | Dissertação |
Idioma: | por |
Título da fonte: | Repositório Institucional da UFG |
Texto Completo: | http://repositorio.bc.ufg.br/tede/handle/tede/5992 |
Resumo: | Previous studies have demonstrated a protective effect of the Ang-(1-7)/Mas receptor axis on pathological cardiac hypertrophy. Also, the involvement of Mas receptor in the exercise-induced cardiac hypertrophy has been suggested. However, the role of the Ang-(1-7)/Mas receptor on pregnancy-induced cardiac remodeling remains unknown. Thus, the aim of this study was to evaluate the participation of the Mas receptor in the development of pregnancy and hypertrophy, fibrosis and cardiac function during pregnancy. Female Wistar rats were randomly shared in 3 groups: control (W-NP), pregnant (W-P), and pregnant treated with A-779 (W-P + A-779). Wild type and Masknockout mice were distributed in non-pregnant (WT and KO) and pregnant (WT-P and KO-P) groups. Gestational parameters such as, maternal weight, placental weight, fetus weight, fetus/placenta ratio, fertility, Loss pre embryonic, Loss pos embryonic were evaluated. Systolic blood pressure (SBP) was measured by tail-cuff plethysmography. The medial part of the left ventricle (LV) was collected for cardiomyocytes morphometry analysis and extracellular matrix proteins deposition. Echocardiographic analysis was used to evaluate the cardiac function. Mas receptor blockade or genetic deletion of Mas did not alter the fertility or embryonic and fetal development. However, the Mas receptor antagonist decreased placental weight and increased fetus placenta ratio in rats. The pregnant KO mice presented a decreased maternal and fetal weight and increased fetus/placenta ratio. SBP was not changed by pregnancy or A-779 treatment in the Wistar rats. Pharmacological blockade or genetic deletion of Mas receptor attenuates the pregnancy-induced myocyte hypertrophy. The A-779 treatment or genetic deletion of the Mas receptor increased the collagen III deposition in LV from pregnant animals. KO mice presented a lower ejection fraction, fraction shortening, stroke volume and higher end systolic volume compared to WT. Interestingly, the pregnancy restored these parameters. In conclusion, these data show that Mas receptor can alter gestational and maternal parameters, and this is involved in the cardiomyocyte hypertrophy and in the control of the collagen III deposition in pregnancy condition. These alterations are associated with improvement of the cardiac function through Mas-independent mechanism. |
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Castro, Carlos Henrique dehttp://lattes.cnpq.br/6354834854727314Costa, Renata Mazaro ehttp://lattes.cnpq.br/5625298314637434Castro, Carlos Henrique dehttp://lattes.cnpq.br/3449243300384555Silva, Cintia do Carmo e2016-08-25T12:21:31Z2016-03-21SILVA, C.C. Receptor Mas contribui para o desenvolvimento do remodelamento cardíaco. 2016. 57 f. Dissertação (Meestrado em Biologia) - Universidade Federal de Goiás, Goiânia, 2016.http://repositorio.bc.ufg.br/tede/handle/tede/5992ark:/38995/0013000000r3sPrevious studies have demonstrated a protective effect of the Ang-(1-7)/Mas receptor axis on pathological cardiac hypertrophy. Also, the involvement of Mas receptor in the exercise-induced cardiac hypertrophy has been suggested. However, the role of the Ang-(1-7)/Mas receptor on pregnancy-induced cardiac remodeling remains unknown. Thus, the aim of this study was to evaluate the participation of the Mas receptor in the development of pregnancy and hypertrophy, fibrosis and cardiac function during pregnancy. Female Wistar rats were randomly shared in 3 groups: control (W-NP), pregnant (W-P), and pregnant treated with A-779 (W-P + A-779). Wild type and Masknockout mice were distributed in non-pregnant (WT and KO) and pregnant (WT-P and KO-P) groups. Gestational parameters such as, maternal weight, placental weight, fetus weight, fetus/placenta ratio, fertility, Loss pre embryonic, Loss pos embryonic were evaluated. Systolic blood pressure (SBP) was measured by tail-cuff plethysmography. The medial part of the left ventricle (LV) was collected for cardiomyocytes morphometry analysis and extracellular matrix proteins deposition. Echocardiographic analysis was used to evaluate the cardiac function. Mas receptor blockade or genetic deletion of Mas did not alter the fertility or embryonic and fetal development. However, the Mas receptor antagonist decreased placental weight and increased fetus placenta ratio in rats. The pregnant KO mice presented a decreased maternal and fetal weight and increased fetus/placenta ratio. SBP was not changed by pregnancy or A-779 treatment in the Wistar rats. Pharmacological blockade or genetic deletion of Mas receptor attenuates the pregnancy-induced myocyte hypertrophy. The A-779 treatment or genetic deletion of the Mas receptor increased the collagen III deposition in LV from pregnant animals. KO mice presented a lower ejection fraction, fraction shortening, stroke volume and higher end systolic volume compared to WT. Interestingly, the pregnancy restored these parameters. In conclusion, these data show that Mas receptor can alter gestational and maternal parameters, and this is involved in the cardiomyocyte hypertrophy and in the control of the collagen III deposition in pregnancy condition. These alterations are associated with improvement of the cardiac function through Mas-independent mechanism.Estudos anteriores mostraram que o eixo Ang- (1-7) / receptor Mas possue efeito protetor na hipertrofia cardíaca patológica. Além disso, o envolvimento de receptor Mas na hipertrofia cardíaca induzida por exercício tem sido sugerida. No entanto, o papel da Ang- (1-7) / receptor Mas no remodelamento cardíaco induzido pela gestação permanece desconhecido. Diante disto, o objetivo desse estudo foi avaliar a participação do receptor Mas no desenvolvimento da gestação e na hipertrofia, fibrose e função cardíaca durante a gestação. Ratas Wistar foram randomizadas aleatoriamente em 3 grupos: controle (W-NP), gestante (W-P) e gestante tratada com A-779 (W-P + A-779). Camundongas Wild type e Knockout para o receptor Mas foram randominazadas em grupos não-grávidas (WT e KO) e grávidas (WT-P e KO-P). Parâmetros gestacionais como peso materno, peso placentário, peso fetal, razão feto/placenta, fertilidade, perda pré-embrionária e perda pós-embrionária foram avaliados. A pressão arterial sistólica (PAS) foi medida por pletismografia de cauda. A parte medial do ventrículo esquerdo (VE) foi coletado para análise morfométrica do cardiomiócito e deposição de proteínas na matriz extracelular. Análise por ecocardiografia foi utilizada para avaliar a função cardíaca. O bloqueio ou a deleção genética do Mas não altera a fertilidade, o desenvolvimento embrionário ou fetal. No entanto, o bloqueio do Mas reduziu o peso placentário e aumentou a relação feto/placenta nas ratas. Já nos animais KO gestantes foi observado menor ganho de peso materno e fetal, o que acarretou em aumento da razão feto/placenta. A PAS não foi alterada pela gestação ou tratamento com A-779 nas ratas Wistar. O bloqueio farmacológico ou deleção genética de receptor Mas atenuou a hipertrofia dos miócitos induzida pela gravidez. O tratamento A-779 ou deleção genética do receptor Mas aumentou a deposição de colágeno III do VE das gestantes. KO apresentaram uma menor fração de ejeção, fração de encurtamento, volume sistólico e aumento do volume sistólico final em comparação com WT. Curiosamente, a gravidez restaurou esses parâmetros. Em conclusão, estes dados demonstraram que o receptor Mas pode alterar parâmetros maternos e gestacionais, bem como está envolvido na hipertrofia dos cardiomiócitos e no controle da deposição de colágeno III na gestação. Essas alterações estão associadas com a melhora da função cardíaca por meio de mecanismos independente do MasSubmitted by Luciana Ferreira (lucgeral@gmail.com) on 2016-08-25T12:21:12Z No. of bitstreams: 2 Dissertação - Cíntia do Carmo e Silva - 2016.pdf: 1705558 bytes, checksum: f3f7616f0bd9d70c3439ec18c38eef3f (MD5) license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5)Approved for entry into archive by Luciana Ferreira (lucgeral@gmail.com) on 2016-08-25T12:21:31Z (GMT) No. of bitstreams: 2 Dissertação - Cíntia do Carmo e Silva - 2016.pdf: 1705558 bytes, checksum: f3f7616f0bd9d70c3439ec18c38eef3f (MD5) license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5)Made available in DSpace on 2016-08-25T12:21:31Z (GMT). No. of bitstreams: 2 Dissertação - Cíntia do Carmo e Silva - 2016.pdf: 1705558 bytes, checksum: f3f7616f0bd9d70c3439ec18c38eef3f (MD5) license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5) Previous issue date: 2016-03-21Fundação de Amparo à Pesquisa do Estado de Goiás - FAPEGapplication/pdfporUniversidade Federal de GoiásPrograma de Pós-graduação em Biologia (ICB)UFGBrasilInstituto de Ciências Biológicas - ICB (RG)http://creativecommons.org/licenses/by-nc-nd/4.0/info:eu-repo/semantics/openAccessAngiotensina- (1-7)Hipertrofia cardíacaFibroseFunção cardíacaA- 779Angiotensin-(1-7)Cardiac hypertrophyFibrosisHeart functionA-779CIENCIAS BIOLOGICAS::FARMACOLOGIAReceptor Mas contribui para o desenvolvimento do remodelamento cardíacoMas receptor contributes to pregnancy-induced cardiacinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/masterThesis6883982777473437920600600600600-3872772117827373404700814650651154363-961409807440757778reponame:Repositório Institucional da UFGinstname:Universidade Federal de Goiás (UFG)instacron:UFGLICENSElicense.txtlicense.txttext/plain; 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dc.title.por.fl_str_mv |
Receptor Mas contribui para o desenvolvimento do remodelamento cardíaco |
dc.title.alternative.eng.fl_str_mv |
Mas receptor contributes to pregnancy-induced cardiac |
title |
Receptor Mas contribui para o desenvolvimento do remodelamento cardíaco |
spellingShingle |
Receptor Mas contribui para o desenvolvimento do remodelamento cardíaco Silva, Cintia do Carmo e Angiotensina- (1-7) Hipertrofia cardíaca Fibrose Função cardíaca A- 779 Angiotensin-(1-7) Cardiac hypertrophy Fibrosis Heart function A-779 CIENCIAS BIOLOGICAS::FARMACOLOGIA |
title_short |
Receptor Mas contribui para o desenvolvimento do remodelamento cardíaco |
title_full |
Receptor Mas contribui para o desenvolvimento do remodelamento cardíaco |
title_fullStr |
Receptor Mas contribui para o desenvolvimento do remodelamento cardíaco |
title_full_unstemmed |
Receptor Mas contribui para o desenvolvimento do remodelamento cardíaco |
title_sort |
Receptor Mas contribui para o desenvolvimento do remodelamento cardíaco |
author |
Silva, Cintia do Carmo e |
author_facet |
Silva, Cintia do Carmo e |
author_role |
author |
dc.contributor.advisor1.fl_str_mv |
Castro, Carlos Henrique de |
dc.contributor.advisor1Lattes.fl_str_mv |
http://lattes.cnpq.br/6354834854727314 |
dc.contributor.advisor-co1.fl_str_mv |
Costa, Renata Mazaro e |
dc.contributor.advisor-co1Lattes.fl_str_mv |
http://lattes.cnpq.br/5625298314637434 |
dc.contributor.referee1.fl_str_mv |
Castro, Carlos Henrique de |
dc.contributor.authorLattes.fl_str_mv |
http://lattes.cnpq.br/3449243300384555 |
dc.contributor.author.fl_str_mv |
Silva, Cintia do Carmo e |
contributor_str_mv |
Castro, Carlos Henrique de Costa, Renata Mazaro e Castro, Carlos Henrique de |
dc.subject.por.fl_str_mv |
Angiotensina- (1-7) Hipertrofia cardíaca Fibrose Função cardíaca A- 779 |
topic |
Angiotensina- (1-7) Hipertrofia cardíaca Fibrose Função cardíaca A- 779 Angiotensin-(1-7) Cardiac hypertrophy Fibrosis Heart function A-779 CIENCIAS BIOLOGICAS::FARMACOLOGIA |
dc.subject.eng.fl_str_mv |
Angiotensin-(1-7) Cardiac hypertrophy Fibrosis Heart function A-779 |
dc.subject.cnpq.fl_str_mv |
CIENCIAS BIOLOGICAS::FARMACOLOGIA |
description |
Previous studies have demonstrated a protective effect of the Ang-(1-7)/Mas receptor axis on pathological cardiac hypertrophy. Also, the involvement of Mas receptor in the exercise-induced cardiac hypertrophy has been suggested. However, the role of the Ang-(1-7)/Mas receptor on pregnancy-induced cardiac remodeling remains unknown. Thus, the aim of this study was to evaluate the participation of the Mas receptor in the development of pregnancy and hypertrophy, fibrosis and cardiac function during pregnancy. Female Wistar rats were randomly shared in 3 groups: control (W-NP), pregnant (W-P), and pregnant treated with A-779 (W-P + A-779). Wild type and Masknockout mice were distributed in non-pregnant (WT and KO) and pregnant (WT-P and KO-P) groups. Gestational parameters such as, maternal weight, placental weight, fetus weight, fetus/placenta ratio, fertility, Loss pre embryonic, Loss pos embryonic were evaluated. Systolic blood pressure (SBP) was measured by tail-cuff plethysmography. The medial part of the left ventricle (LV) was collected for cardiomyocytes morphometry analysis and extracellular matrix proteins deposition. Echocardiographic analysis was used to evaluate the cardiac function. Mas receptor blockade or genetic deletion of Mas did not alter the fertility or embryonic and fetal development. However, the Mas receptor antagonist decreased placental weight and increased fetus placenta ratio in rats. The pregnant KO mice presented a decreased maternal and fetal weight and increased fetus/placenta ratio. SBP was not changed by pregnancy or A-779 treatment in the Wistar rats. Pharmacological blockade or genetic deletion of Mas receptor attenuates the pregnancy-induced myocyte hypertrophy. The A-779 treatment or genetic deletion of the Mas receptor increased the collagen III deposition in LV from pregnant animals. KO mice presented a lower ejection fraction, fraction shortening, stroke volume and higher end systolic volume compared to WT. Interestingly, the pregnancy restored these parameters. In conclusion, these data show that Mas receptor can alter gestational and maternal parameters, and this is involved in the cardiomyocyte hypertrophy and in the control of the collagen III deposition in pregnancy condition. These alterations are associated with improvement of the cardiac function through Mas-independent mechanism. |
publishDate |
2016 |
dc.date.accessioned.fl_str_mv |
2016-08-25T12:21:31Z |
dc.date.issued.fl_str_mv |
2016-03-21 |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/masterThesis |
format |
masterThesis |
status_str |
publishedVersion |
dc.identifier.citation.fl_str_mv |
SILVA, C.C. Receptor Mas contribui para o desenvolvimento do remodelamento cardíaco. 2016. 57 f. Dissertação (Meestrado em Biologia) - Universidade Federal de Goiás, Goiânia, 2016. |
dc.identifier.uri.fl_str_mv |
http://repositorio.bc.ufg.br/tede/handle/tede/5992 |
dc.identifier.dark.fl_str_mv |
ark:/38995/0013000000r3s |
identifier_str_mv |
SILVA, C.C. Receptor Mas contribui para o desenvolvimento do remodelamento cardíaco. 2016. 57 f. Dissertação (Meestrado em Biologia) - Universidade Federal de Goiás, Goiânia, 2016. ark:/38995/0013000000r3s |
url |
http://repositorio.bc.ufg.br/tede/handle/tede/5992 |
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por |
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por |
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6883982777473437920 |
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600 600 600 600 |
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700814650651154363 |
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http://creativecommons.org/licenses/by-nc-nd/4.0/ info:eu-repo/semantics/openAccess |
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http://creativecommons.org/licenses/by-nc-nd/4.0/ |
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Universidade Federal de Goiás |
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UFG |
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Brasil |
dc.publisher.department.fl_str_mv |
Instituto de Ciências Biológicas - ICB (RG) |
publisher.none.fl_str_mv |
Universidade Federal de Goiás |
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Repositório Institucional da UFG - Universidade Federal de Goiás (UFG) |
repository.mail.fl_str_mv |
tasesdissertacoes.bc@ufg.br |
_version_ |
1811721322698375168 |