Reatividade da astroglia durante o desenvolvimento da retina de ratos submetidos a um modelo de hipóxia-isquemia pré-natal
Autor(a) principal: | |
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Data de Publicação: | 2019 |
Outros Autores: | |
Tipo de documento: | Dissertação |
Idioma: | por |
Título da fonte: | Biblioteca Digital de Teses e Dissertações da UERJ |
Texto Completo: | http://www.bdtd.uerj.br/handle/1/20312 |
Resumo: | The hypoxic-ischemic insult (HI) is responsible for several CNS compromises during its development or at adulthood. Its consequences can cause varying degrees of retinopathy and visual impairment. Thus, investigating the effects of this insult on the retina may help to elucidate the mechanisms responsible for the consequences and thus outline therapeutical approaches. This work sought to mimic the most common human event, which occurs prenatally and may be irreversible. Using a model in which the uterine and ovarian flow of the pregnant rat is obstructed for 45 minutes on the 18th gestational day, a decrease in the optic nerve thickness and in the retinal projections in the dorsal lateral geniculate nucleus (NGLd), GCL loss and failure to maintain pupillary constriction have been reported. The aim of this study was to evaluate the retinal glial reactivity of Wistar rats during development (at two, nine, twenty three and thirteen postnatal days). The surgery for HI induction was performed with obstruction of uterine and ovarian flow (HI group) for 45 minutes on the eighteenth day of gestation. Animals that underwent all surgical procedure except for obstruction of blood flow constitute the sham-operated group (SH). Histological evaluation was performed to evaluate the development and response to the HI insult in cells of the retinal astroglial lineage, astrocytes and Muller's glia, using immunohistochemistry for glial fibrillary acidic protein (GFAP) and vimentin (VIM). Immunostaining for the GLAST glutamate transporter was also evaluated. The results showed that HI insult promotes an increase in GFAP and VIM labeling on the thirtieth postnatal day, as well as alters the immunostaining pattern for the GLAST transporter by anticipating the peak of labeling to the ninth day in the HI group. Taken together, the results show that, also in the retina, a gliosis occurs, as also described in other brain regions in rats submitted to this prenatal HI model. In addition to the results obtained for the GLAST transporter, we reinforce the hypothesis that glutamate transport alterations may contribute to glutamatergic excitotoxicity, one of the events responsible for neuronal death in this kind of lesion. Once more, we showed that the prenatal HI model used in this study is an important tool to be used in order to understand the mechanisms of the lesions caused by HI during development, as well as for the evaluation of possible therapeutic strategies. |
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Krahe, Thomas Eichenberghttp://lattes.cnpq.br/5280805567151610Santos, Penha Cristina Barradas Daltrohttp://lattes.cnpq.br/9817163660114748Villaça, Yael de Abreuhttp://lattes.cnpq.br/2110538573461886Araújo, Elizabeth Giestal dehttp://lattes.cnpq.br/8230334072312477Calaza, Karin da Costahttp://lattes.cnpq.br/5859948736421528http://lattes.cnpq.br/3605728417381849Fonseca, Lara Silvaisf_lara@hotmail.com2023-09-19T13:01:48Z2019-08-30FONSECA, Lara Silva. Reatividade da astroglia durante o desenvolvimento da retina de ratos submetidos a um modelo de hipóxia-isquemia pré-natal. 2019. 91 f. Dissertação (Mestrado em Fisiopatologia Clínica e Experimental) – Faculdade de Ciências Médicas, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, 2019.http://www.bdtd.uerj.br/handle/1/20312The hypoxic-ischemic insult (HI) is responsible for several CNS compromises during its development or at adulthood. Its consequences can cause varying degrees of retinopathy and visual impairment. Thus, investigating the effects of this insult on the retina may help to elucidate the mechanisms responsible for the consequences and thus outline therapeutical approaches. This work sought to mimic the most common human event, which occurs prenatally and may be irreversible. Using a model in which the uterine and ovarian flow of the pregnant rat is obstructed for 45 minutes on the 18th gestational day, a decrease in the optic nerve thickness and in the retinal projections in the dorsal lateral geniculate nucleus (NGLd), GCL loss and failure to maintain pupillary constriction have been reported. The aim of this study was to evaluate the retinal glial reactivity of Wistar rats during development (at two, nine, twenty three and thirteen postnatal days). The surgery for HI induction was performed with obstruction of uterine and ovarian flow (HI group) for 45 minutes on the eighteenth day of gestation. Animals that underwent all surgical procedure except for obstruction of blood flow constitute the sham-operated group (SH). Histological evaluation was performed to evaluate the development and response to the HI insult in cells of the retinal astroglial lineage, astrocytes and Muller's glia, using immunohistochemistry for glial fibrillary acidic protein (GFAP) and vimentin (VIM). Immunostaining for the GLAST glutamate transporter was also evaluated. The results showed that HI insult promotes an increase in GFAP and VIM labeling on the thirtieth postnatal day, as well as alters the immunostaining pattern for the GLAST transporter by anticipating the peak of labeling to the ninth day in the HI group. Taken together, the results show that, also in the retina, a gliosis occurs, as also described in other brain regions in rats submitted to this prenatal HI model. In addition to the results obtained for the GLAST transporter, we reinforce the hypothesis that glutamate transport alterations may contribute to glutamatergic excitotoxicity, one of the events responsible for neuronal death in this kind of lesion. Once more, we showed that the prenatal HI model used in this study is an important tool to be used in order to understand the mechanisms of the lesions caused by HI during development, as well as for the evaluation of possible therapeutic strategies.O insulto hipóxico-isquêmico (HI) é o responsável por diversos comprometimentos no SNC, durante o seu desenvolvimento ou na fase adulta. Suas consequências podem causar diversos graus de retinopatias e deficiências visuais. Dessa forma, investigar os efeitos desse insulto na retina pode auxiliar a elucidar os mecanismos responsáveis pelas consequências e assim traçar medidas terapêuticas. Esse trabalho buscou mimetizar o evento mais ocorrido em humanos, que ocorre de forma pré-natal e pode ser irreversível. Utilizando um modelo em que o fluxo uterino e ovariano da rata grávida é obstruído por 45 minutos no 18º dia gestacional, já foi relatada diminuição da espessura do nervo óptico e das projeções retinianas no Núcleo Geniculado Lateral dorsal (NGLd), perda de CCG e a não manutenção da constrição pupilar. Neste trabalho, o objetivo foi avaliar a reatividade glial na retina de ratos Wistar durante o desenvolvimento (aos dois, nove, vinte e três e trinta dias pós-natal). Foi realizado o procedimento cirúrgico de indução de HI com a obstrução do fluxo uterino e ovariano (grupo HI) por 45 minutos no décimo oitavo dia da gestação. Animais que passaram por todo procedimento cirúrgico exceto pela obstrução do fluxo sanguíneo constituem o grupo falso operado (SH). Foi realizada a avaliação histológica com o objetivo de avaliar o desenvolvimento e a resposta ao insulto HI nas células da linhagem astroglial da retina, astrócitos e glia de Muller, utilizando a imunohistoquímica para a proteína glial fibrilar ácida (GFAP) e para a vimentina (VIM). Também foi avaliada a imunomarcação para o transportador de glutamato GLAST. Os resultados obtidos mostraram que o insulto HI promove um aumento da marcação de GFAP e VIM no trigésimo dia pós-natal, bem como altera a padrão de imunomarcação para o transportador GLAST, antecipando o pico de marcação para a idade de nove dias no grupo HI. Em conjunto, os resultados mostram que também na retina ocorre a gliose já relatada em outras regiões do encéfalo de animais submetidos a esse modelo de HI pré-natal. Somados aos resultados obtidos referentes ao transportador GLAST, reforçamos a hipótese de alterações no transporte de glutamato que podem contribuir para a excitotoxicidade glutamatérgica, um dos eventos responsáveis pela morte neuronal oriunda dessa lesão. O modelo de HI pré-natal desenvolvido nesse trabalho, mais uma vez, se mostra uma ferramenta importante para o estudo das lesões causadas pela HI durante o desenvolvimento, assim como para a avaliação de possíveis estratégias terapêuticas.Submitted by Heloísa CB/A (helobdtd@gmail.com) on 2023-09-19T13:01:48Z No. of bitstreams: 1 Dissertação - Lara Silva Fonseca - 2019 - Completa.pdf: 1708128 bytes, checksum: d404070f7035788168f51c024f8a991f (MD5)Made available in DSpace on 2023-09-19T13:01:48Z (GMT). No. of bitstreams: 1 Dissertação - Lara Silva Fonseca - 2019 - Completa.pdf: 1708128 bytes, checksum: d404070f7035788168f51c024f8a991f (MD5) Previous issue date: 2019-08-30Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - CAPESapplication/pdfporUniversidade do Estado do Rio de JaneiroPrograma de Pós-Graduação em Fisiopatologia Clínica e ExperimentalUERJBrasilCentro Biomédico::Instituto de Biologia Roberto Alcantara GomesPrenatal hypoxia-ischemiaRetinaDevelopmentGliosisGLASTHipóxia-isquemia pré-natalRetinaDesenvolvimentoGlioseGLASTCIENCIAS BIOLOGICAS::FISIOLOGIA::FISIOLOGIA GERALReatividade da astroglia durante o desenvolvimento da retina de ratos submetidos a um modelo de hipóxia-isquemia pré-natalAstroglial reactivity during retinal development of rats submitted to a prenatal hypoxia-ischemia modelinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/masterThesisinfo:eu-repo/semantics/openAccessreponame:Biblioteca Digital de Teses e Dissertações da UERJinstname:Universidade do Estado do Rio de Janeiro (UERJ)instacron:UERJORIGINALDissertação - Lara Silva Fonseca - 2019 - Completa.pdfDissertação - Lara Silva Fonseca - 2019 - Completa.pdfapplication/pdf1708128http://www.bdtd.uerj.br/bitstream/1/20312/2/Disserta%C3%A7%C3%A3o+-+Lara+Silva+Fonseca+-+2019+-+Completa.pdfd404070f7035788168f51c024f8a991fMD52LICENSElicense.txtlicense.txttext/plain; charset=utf-82123http://www.bdtd.uerj.br/bitstream/1/20312/1/license.txte5502652da718045d7fcd832b79fca29MD511/203122024-02-26 16:36:27.148oai:www.bdtd.uerj.br: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Biblioteca Digital de Teses e Dissertaçõeshttp://www.bdtd.uerj.br/PUBhttps://www.bdtd.uerj.br:8443/oai/requestbdtd.suporte@uerj.bropendoar:29032024-02-26T19:36:27Biblioteca Digital de Teses e Dissertações da UERJ - Universidade do Estado do Rio de Janeiro (UERJ)false |
dc.title.por.fl_str_mv |
Reatividade da astroglia durante o desenvolvimento da retina de ratos submetidos a um modelo de hipóxia-isquemia pré-natal |
dc.title.alternative.eng.fl_str_mv |
Astroglial reactivity during retinal development of rats submitted to a prenatal hypoxia-ischemia model |
title |
Reatividade da astroglia durante o desenvolvimento da retina de ratos submetidos a um modelo de hipóxia-isquemia pré-natal |
spellingShingle |
Reatividade da astroglia durante o desenvolvimento da retina de ratos submetidos a um modelo de hipóxia-isquemia pré-natal Fonseca, Lara Silva Prenatal hypoxia-ischemia Retina Development Gliosis GLAST Hipóxia-isquemia pré-natal Retina Desenvolvimento Gliose GLAST CIENCIAS BIOLOGICAS::FISIOLOGIA::FISIOLOGIA GERAL |
title_short |
Reatividade da astroglia durante o desenvolvimento da retina de ratos submetidos a um modelo de hipóxia-isquemia pré-natal |
title_full |
Reatividade da astroglia durante o desenvolvimento da retina de ratos submetidos a um modelo de hipóxia-isquemia pré-natal |
title_fullStr |
Reatividade da astroglia durante o desenvolvimento da retina de ratos submetidos a um modelo de hipóxia-isquemia pré-natal |
title_full_unstemmed |
Reatividade da astroglia durante o desenvolvimento da retina de ratos submetidos a um modelo de hipóxia-isquemia pré-natal |
title_sort |
Reatividade da astroglia durante o desenvolvimento da retina de ratos submetidos a um modelo de hipóxia-isquemia pré-natal |
author |
Fonseca, Lara Silva |
author_facet |
Fonseca, Lara Silva isf_lara@hotmail.com |
author_role |
author |
author2 |
isf_lara@hotmail.com |
author2_role |
author |
dc.contributor.advisor1.fl_str_mv |
Krahe, Thomas Eichenberg |
dc.contributor.advisor1Lattes.fl_str_mv |
http://lattes.cnpq.br/5280805567151610 |
dc.contributor.advisor-co1.fl_str_mv |
Santos, Penha Cristina Barradas Daltro |
dc.contributor.advisor-co1Lattes.fl_str_mv |
http://lattes.cnpq.br/9817163660114748 |
dc.contributor.referee1.fl_str_mv |
Villaça, Yael de Abreu |
dc.contributor.referee1Lattes.fl_str_mv |
http://lattes.cnpq.br/2110538573461886 |
dc.contributor.referee2.fl_str_mv |
Araújo, Elizabeth Giestal de |
dc.contributor.referee2Lattes.fl_str_mv |
http://lattes.cnpq.br/8230334072312477 |
dc.contributor.referee3.fl_str_mv |
Calaza, Karin da Costa |
dc.contributor.referee3Lattes.fl_str_mv |
http://lattes.cnpq.br/5859948736421528 |
dc.contributor.authorLattes.fl_str_mv |
http://lattes.cnpq.br/3605728417381849 |
dc.contributor.author.fl_str_mv |
Fonseca, Lara Silva isf_lara@hotmail.com |
contributor_str_mv |
Krahe, Thomas Eichenberg Santos, Penha Cristina Barradas Daltro Villaça, Yael de Abreu Araújo, Elizabeth Giestal de Calaza, Karin da Costa |
dc.subject.eng.fl_str_mv |
Prenatal hypoxia-ischemia Retina Development Gliosis GLAST |
topic |
Prenatal hypoxia-ischemia Retina Development Gliosis GLAST Hipóxia-isquemia pré-natal Retina Desenvolvimento Gliose GLAST CIENCIAS BIOLOGICAS::FISIOLOGIA::FISIOLOGIA GERAL |
dc.subject.por.fl_str_mv |
Hipóxia-isquemia pré-natal Retina Desenvolvimento Gliose GLAST |
dc.subject.cnpq.fl_str_mv |
CIENCIAS BIOLOGICAS::FISIOLOGIA::FISIOLOGIA GERAL |
description |
The hypoxic-ischemic insult (HI) is responsible for several CNS compromises during its development or at adulthood. Its consequences can cause varying degrees of retinopathy and visual impairment. Thus, investigating the effects of this insult on the retina may help to elucidate the mechanisms responsible for the consequences and thus outline therapeutical approaches. This work sought to mimic the most common human event, which occurs prenatally and may be irreversible. Using a model in which the uterine and ovarian flow of the pregnant rat is obstructed for 45 minutes on the 18th gestational day, a decrease in the optic nerve thickness and in the retinal projections in the dorsal lateral geniculate nucleus (NGLd), GCL loss and failure to maintain pupillary constriction have been reported. The aim of this study was to evaluate the retinal glial reactivity of Wistar rats during development (at two, nine, twenty three and thirteen postnatal days). The surgery for HI induction was performed with obstruction of uterine and ovarian flow (HI group) for 45 minutes on the eighteenth day of gestation. Animals that underwent all surgical procedure except for obstruction of blood flow constitute the sham-operated group (SH). Histological evaluation was performed to evaluate the development and response to the HI insult in cells of the retinal astroglial lineage, astrocytes and Muller's glia, using immunohistochemistry for glial fibrillary acidic protein (GFAP) and vimentin (VIM). Immunostaining for the GLAST glutamate transporter was also evaluated. The results showed that HI insult promotes an increase in GFAP and VIM labeling on the thirtieth postnatal day, as well as alters the immunostaining pattern for the GLAST transporter by anticipating the peak of labeling to the ninth day in the HI group. Taken together, the results show that, also in the retina, a gliosis occurs, as also described in other brain regions in rats submitted to this prenatal HI model. In addition to the results obtained for the GLAST transporter, we reinforce the hypothesis that glutamate transport alterations may contribute to glutamatergic excitotoxicity, one of the events responsible for neuronal death in this kind of lesion. Once more, we showed that the prenatal HI model used in this study is an important tool to be used in order to understand the mechanisms of the lesions caused by HI during development, as well as for the evaluation of possible therapeutic strategies. |
publishDate |
2019 |
dc.date.issued.fl_str_mv |
2019-08-30 |
dc.date.accessioned.fl_str_mv |
2023-09-19T13:01:48Z |
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 |
FONSECA, Lara Silva. Reatividade da astroglia durante o desenvolvimento da retina de ratos submetidos a um modelo de hipóxia-isquemia pré-natal. 2019. 91 f. Dissertação (Mestrado em Fisiopatologia Clínica e Experimental) – Faculdade de Ciências Médicas, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, 2019. |
dc.identifier.uri.fl_str_mv |
http://www.bdtd.uerj.br/handle/1/20312 |
identifier_str_mv |
FONSECA, Lara Silva. Reatividade da astroglia durante o desenvolvimento da retina de ratos submetidos a um modelo de hipóxia-isquemia pré-natal. 2019. 91 f. Dissertação (Mestrado em Fisiopatologia Clínica e Experimental) – Faculdade de Ciências Médicas, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, 2019. |
url |
http://www.bdtd.uerj.br/handle/1/20312 |
dc.language.iso.fl_str_mv |
por |
language |
por |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
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application/pdf |
dc.publisher.none.fl_str_mv |
Universidade do Estado do Rio de Janeiro |
dc.publisher.program.fl_str_mv |
Programa de Pós-Graduação em Fisiopatologia Clínica e Experimental |
dc.publisher.initials.fl_str_mv |
UERJ |
dc.publisher.country.fl_str_mv |
Brasil |
dc.publisher.department.fl_str_mv |
Centro Biomédico::Instituto de Biologia Roberto Alcantara Gomes |
publisher.none.fl_str_mv |
Universidade do Estado do Rio de Janeiro |
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Biblioteca Digital de Teses e Dissertações da UERJ |
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