Kisspeptin treatment improves fetal-placental development and blocks placental oxidative damage caused by maternal hypothyroidism in an experimental rat model
Autor(a) principal: | |
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Data de Publicação: | 2022 |
Outros Autores: | , , , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | por |
Título da fonte: | Repositório Institucional da UFMG |
Texto Completo: | https://doi.org/10.3389/fendo.2022.908240 http://hdl.handle.net/1843/60273 https://orcid.org/0000-0001-7587-6662 https://orcid.org/0000-0001-5374-6242 https://orcid.org/0000-0002-9881-1236 https://orcid.org/0000-0002-7209-6043 https://orcid.org/0000-0001-7679-1353 https://orcid.org/0000-0002-5620-6273 https://orcid.org/0000-0003-0795-5320 https://orcid.org/0000-0002-2639-3469 |
Resumo: | Maternal hypothyroidism is associated with fetal growth restriction, placental dysfunction, and reduced kisspeptin/Kiss1R at the maternal-fetal interface. Kisspeptin affects trophoblastic migration and has antioxidant and immunomodulatory activities. This study aimed to evaluate the therapeutic potential of kisspeptin in the fetal-placental dysfunction of hypothyroid Wistar rats. Hypothyroidism was induced by daily administration of propylthiouracil. Kisspeptin-10 (Kp-10) treatment was performed every other day or daily beginning on day 8 of gestation. Feto-placental development, placental histomorphometry, and expression levels of growth factors (VEGF, PLGF, IGF1, IGF2, and GLUT1), hormonal (Dio2) and inflammatory mediators (TNFα, IL10, and IL6), markers of hypoxia (HIF1α) and oxidative damage (8-OHdG), antioxidant enzymes (SOD1, Cat, and GPx1), and endoplasmic reticulum stress mediators (ATF4, GRP78, and CHOP) were evaluated on day 18 of gestation. Daily treatment with Kp-10 increased free T3 and T4 levels and improved fetal weight. Both treatments reestablished the glycogen cell population in the junctional zone. Daily treatment with Kp-10 increased the gene expression levels of Plgf, Igf1, and Glut1 in the placenta of hypothyroid animals, in addition to blocking the increase in 8-OHdG and increasing protein and/or mRNA expression levels of SOD1, Cat, and GPx1. Daily treatment with Kp-10 did not alter the higher protein expression levels of VEGF, HIF1α, IL10, GRP78, and CHOP caused by hypothyroidism in the junctional zone compared to control, nor the lower expression of Dio2 caused by hypothyroidism. However, in the labyrinth zone, this treatment restored the expression of VEGF and IL10 and reduced the GRP78 and CHOP immunostaining. These findings demonstrate that daily treatment with Kp-10 improves fetal development and placental morphology in hypothyroid rats, blocks placental oxidative damage, and increases the expression of growth factors and antioxidant enzymes in the placenta. |
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2023-10-30T20:57:57Z2023-10-30T20:57:57Z202213118https://doi.org/10.3389/fendo.2022.9082401664-2392http://hdl.handle.net/1843/60273https://orcid.org/0000-0001-7587-6662https://orcid.org/0000-0001-5374-6242https://orcid.org/0000-0002-9881-1236https://orcid.org/0000-0002-7209-6043https://orcid.org/0000-0001-7679-1353https://orcid.org/0000-0002-5620-6273https://orcid.org/0000-0003-0795-5320https://orcid.org/0000-0002-2639-3469Maternal hypothyroidism is associated with fetal growth restriction, placental dysfunction, and reduced kisspeptin/Kiss1R at the maternal-fetal interface. Kisspeptin affects trophoblastic migration and has antioxidant and immunomodulatory activities. This study aimed to evaluate the therapeutic potential of kisspeptin in the fetal-placental dysfunction of hypothyroid Wistar rats. Hypothyroidism was induced by daily administration of propylthiouracil. Kisspeptin-10 (Kp-10) treatment was performed every other day or daily beginning on day 8 of gestation. Feto-placental development, placental histomorphometry, and expression levels of growth factors (VEGF, PLGF, IGF1, IGF2, and GLUT1), hormonal (Dio2) and inflammatory mediators (TNFα, IL10, and IL6), markers of hypoxia (HIF1α) and oxidative damage (8-OHdG), antioxidant enzymes (SOD1, Cat, and GPx1), and endoplasmic reticulum stress mediators (ATF4, GRP78, and CHOP) were evaluated on day 18 of gestation. Daily treatment with Kp-10 increased free T3 and T4 levels and improved fetal weight. Both treatments reestablished the glycogen cell population in the junctional zone. Daily treatment with Kp-10 increased the gene expression levels of Plgf, Igf1, and Glut1 in the placenta of hypothyroid animals, in addition to blocking the increase in 8-OHdG and increasing protein and/or mRNA expression levels of SOD1, Cat, and GPx1. Daily treatment with Kp-10 did not alter the higher protein expression levels of VEGF, HIF1α, IL10, GRP78, and CHOP caused by hypothyroidism in the junctional zone compared to control, nor the lower expression of Dio2 caused by hypothyroidism. However, in the labyrinth zone, this treatment restored the expression of VEGF and IL10 and reduced the GRP78 and CHOP immunostaining. These findings demonstrate that daily treatment with Kp-10 improves fetal development and placental morphology in hypothyroid rats, blocks placental oxidative damage, and increases the expression of growth factors and antioxidant enzymes in the placenta.O hipotireoidismo materno está associado à restrição do crescimento fetal, disfunção placentária e redução da kisspeptina/Kiss1R na interface materno-fetal. A Kisspeptina afeta a migração trofoblástica e possui atividades antioxidantes e imunomoduladoras. Este estudo teve como objetivo avaliar o potencial terapêutico da kisspeptina na disfunção feto-placentária de ratos Wistar hipotireoidianos. O hipotireoidismo foi induzido pela administração diária de propiltiouracil. O tratamento com Kisspeptina-10 (Kp-10) foi realizado em dias alternados ou diariamente, começando no 8º dia de gestação. Desenvolvimento feto-placentário, histomorfometria placentária e níveis de expressão de fatores de crescimento (VEGF, PLGF, IGF1, IGF2 e GLUT1), mediadores hormonais (Dio2) e inflamatórios (TNFα, IL10 e IL6), marcadores de hipóxia (HIF1α) e dano oxidativo (8-OHdG), enzimas antioxidantes (SOD1, Cat e GPx1) e mediadores de estresse do retículo endoplasmático (ATF4, GRP78 e CHOP) foram avaliados no 18º dia de gestação. O tratamento diário com Kp-10 aumentou os níveis de T3 e T4 livres e melhorou o peso fetal. Ambos os tratamentos restabeleceram a população de células de glicogênio na zona juncional. O tratamento diário com Kp-10 aumentou os níveis de expressão gênica de Plgf, Igf1 e Glut1 na placenta de animais hipotireoidianos além de bloquear o aumento de 8-OHdG e aumentar os níveis de expressão proteica e/ou mRNA de SOD1, Cat e GPx1. O tratamento diário com Kp-10 não alterou os níveis mais elevados de expressão proteica de VEGF, HIF1α, IL10, GRP78 e CHOP causados pelo hipotireoidismo na zona juncional em comparação ao controle, nem a menor expressão de Dio2 causada pelo hipotireoidismo. Porém, na zona do labirinto, este tratamento restaurou a expressão de VEGF e IL10 e reduziu a imunomarcação de GRP78 e CHOP. Estas descobertas demonstram que o tratamento diário com Kp-10 melhora o desenvolvimento fetal e a morfologia placentária em ratos com hipotireoidismo, bloqueia o dano oxidativo placentário e aumenta a expressão de fatores de crescimento e enzimas antioxidantes na placenta.CNPq - Conselho Nacional de Desenvolvimento Científico e TecnológicoCAPES - Coordenação de Aperfeiçoamento de Pessoal de Nível SuperiorOutra AgênciaporUniversidade Federal de Minas GeraisUFMGBrasilICB - DEPARTAMENTO DE FISIOLOGIA E BIOFÍSICAVET - DEPARTAMENTO DE CLÍNICA E CIRURGIAFrontiers in endocrinologyKisspeptinasTrofoblastosGlândula TireoideDesenvolvimento fetalHipertireoidismoKisspeptinTrophoblastThyroidCell stressInflammationFetal developmentRatKisspeptin treatment improves fetal-placental development and blocks placental oxidative damage caused by maternal hypothyroidism in an experimental rat modelO tratamento com Kisspeptina melhora o desenvolvimento fetal-placentário e bloqueia o dano oxidativo placentário causado pelo hipotireoidismo materno em um modelo experimental com ratosinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlehttps://www.frontiersin.org/articles/10.3389/fendo.2022.908240/fullBianca Reis SantosRogéria SerakidesJuneo de Freitas SilvaJeane Martinha dos Anjos CordeiroLuciano Cardoso SantosErikles Macêdo BarbosaLeticia Dias MendonçaEmilly Oliveira SantosIsabella Oliveira de MacedoMario Sérgio Lima de LavorRaphael Escorsim Szawkaapplication/pdfinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UFMGinstname:Universidade Federal de Minas Gerais (UFMG)instacron:UFMGLICENSELicense.txtLicense.txttext/plain; charset=utf-82042https://repositorio.ufmg.br/bitstream/1843/60273/1/License.txtfa505098d172de0bc8864fc1287ffe22MD51ORIGINALKisspeptin treatment improves fetal-placental development and blocks placental oxidative damage caused by maternal hypothyroidism in an experimental rat model.pdfKisspeptin treatment improves fetal-placental development and blocks placental oxidative damage caused by maternal hypothyroidism in an experimental rat model.pdfapplication/pdf13817268https://repositorio.ufmg.br/bitstream/1843/60273/2/Kisspeptin%20treatment%20improves%20fetal-placental%20development%20and%20blocks%20placental%20oxidative%20damage%20caused%20by%20maternal%20hypothyroidism%20in%20an%20experimental%20rat%20model.pdf6ab6a4473bb606fb2872598848debec3MD521843/602732023-10-30 17:57:57.653oai:repositorio.ufmg.br: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Repositório de PublicaçõesPUBhttps://repositorio.ufmg.br/oaiopendoar:2023-10-30T20:57:57Repositório Institucional da UFMG - Universidade Federal de Minas Gerais (UFMG)false |
dc.title.pt_BR.fl_str_mv |
Kisspeptin treatment improves fetal-placental development and blocks placental oxidative damage caused by maternal hypothyroidism in an experimental rat model |
dc.title.alternative.pt_BR.fl_str_mv |
O tratamento com Kisspeptina melhora o desenvolvimento fetal-placentário e bloqueia o dano oxidativo placentário causado pelo hipotireoidismo materno em um modelo experimental com ratos |
title |
Kisspeptin treatment improves fetal-placental development and blocks placental oxidative damage caused by maternal hypothyroidism in an experimental rat model |
spellingShingle |
Kisspeptin treatment improves fetal-placental development and blocks placental oxidative damage caused by maternal hypothyroidism in an experimental rat model Bianca Reis Santos Kisspeptin Trophoblast Thyroid Cell stress Inflammation Fetal development Rat Kisspeptinas Trofoblastos Glândula Tireoide Desenvolvimento fetal Hipertireoidismo |
title_short |
Kisspeptin treatment improves fetal-placental development and blocks placental oxidative damage caused by maternal hypothyroidism in an experimental rat model |
title_full |
Kisspeptin treatment improves fetal-placental development and blocks placental oxidative damage caused by maternal hypothyroidism in an experimental rat model |
title_fullStr |
Kisspeptin treatment improves fetal-placental development and blocks placental oxidative damage caused by maternal hypothyroidism in an experimental rat model |
title_full_unstemmed |
Kisspeptin treatment improves fetal-placental development and blocks placental oxidative damage caused by maternal hypothyroidism in an experimental rat model |
title_sort |
Kisspeptin treatment improves fetal-placental development and blocks placental oxidative damage caused by maternal hypothyroidism in an experimental rat model |
author |
Bianca Reis Santos |
author_facet |
Bianca Reis Santos Rogéria Serakides Juneo de Freitas Silva Jeane Martinha dos Anjos Cordeiro Luciano Cardoso Santos Erikles Macêdo Barbosa Leticia Dias Mendonça Emilly Oliveira Santos Isabella Oliveira de Macedo Mario Sérgio Lima de Lavor Raphael Escorsim Szawka |
author_role |
author |
author2 |
Rogéria Serakides Juneo de Freitas Silva Jeane Martinha dos Anjos Cordeiro Luciano Cardoso Santos Erikles Macêdo Barbosa Leticia Dias Mendonça Emilly Oliveira Santos Isabella Oliveira de Macedo Mario Sérgio Lima de Lavor Raphael Escorsim Szawka |
author2_role |
author author author author author author author author author author |
dc.contributor.author.fl_str_mv |
Bianca Reis Santos Rogéria Serakides Juneo de Freitas Silva Jeane Martinha dos Anjos Cordeiro Luciano Cardoso Santos Erikles Macêdo Barbosa Leticia Dias Mendonça Emilly Oliveira Santos Isabella Oliveira de Macedo Mario Sérgio Lima de Lavor Raphael Escorsim Szawka |
dc.subject.por.fl_str_mv |
Kisspeptin Trophoblast Thyroid Cell stress Inflammation Fetal development Rat |
topic |
Kisspeptin Trophoblast Thyroid Cell stress Inflammation Fetal development Rat Kisspeptinas Trofoblastos Glândula Tireoide Desenvolvimento fetal Hipertireoidismo |
dc.subject.other.pt_BR.fl_str_mv |
Kisspeptinas Trofoblastos Glândula Tireoide Desenvolvimento fetal Hipertireoidismo |
description |
Maternal hypothyroidism is associated with fetal growth restriction, placental dysfunction, and reduced kisspeptin/Kiss1R at the maternal-fetal interface. Kisspeptin affects trophoblastic migration and has antioxidant and immunomodulatory activities. This study aimed to evaluate the therapeutic potential of kisspeptin in the fetal-placental dysfunction of hypothyroid Wistar rats. Hypothyroidism was induced by daily administration of propylthiouracil. Kisspeptin-10 (Kp-10) treatment was performed every other day or daily beginning on day 8 of gestation. Feto-placental development, placental histomorphometry, and expression levels of growth factors (VEGF, PLGF, IGF1, IGF2, and GLUT1), hormonal (Dio2) and inflammatory mediators (TNFα, IL10, and IL6), markers of hypoxia (HIF1α) and oxidative damage (8-OHdG), antioxidant enzymes (SOD1, Cat, and GPx1), and endoplasmic reticulum stress mediators (ATF4, GRP78, and CHOP) were evaluated on day 18 of gestation. Daily treatment with Kp-10 increased free T3 and T4 levels and improved fetal weight. Both treatments reestablished the glycogen cell population in the junctional zone. Daily treatment with Kp-10 increased the gene expression levels of Plgf, Igf1, and Glut1 in the placenta of hypothyroid animals, in addition to blocking the increase in 8-OHdG and increasing protein and/or mRNA expression levels of SOD1, Cat, and GPx1. Daily treatment with Kp-10 did not alter the higher protein expression levels of VEGF, HIF1α, IL10, GRP78, and CHOP caused by hypothyroidism in the junctional zone compared to control, nor the lower expression of Dio2 caused by hypothyroidism. However, in the labyrinth zone, this treatment restored the expression of VEGF and IL10 and reduced the GRP78 and CHOP immunostaining. These findings demonstrate that daily treatment with Kp-10 improves fetal development and placental morphology in hypothyroid rats, blocks placental oxidative damage, and increases the expression of growth factors and antioxidant enzymes in the placenta. |
publishDate |
2022 |
dc.date.issued.fl_str_mv |
2022 |
dc.date.accessioned.fl_str_mv |
2023-10-30T20:57:57Z |
dc.date.available.fl_str_mv |
2023-10-30T20:57:57Z |
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.uri.fl_str_mv |
http://hdl.handle.net/1843/60273 |
dc.identifier.doi.pt_BR.fl_str_mv |
https://doi.org/10.3389/fendo.2022.908240 |
dc.identifier.issn.pt_BR.fl_str_mv |
1664-2392 |
dc.identifier.orcid.pt_BR.fl_str_mv |
https://orcid.org/0000-0001-7587-6662 https://orcid.org/0000-0001-5374-6242 https://orcid.org/0000-0002-9881-1236 https://orcid.org/0000-0002-7209-6043 https://orcid.org/0000-0001-7679-1353 https://orcid.org/0000-0002-5620-6273 https://orcid.org/0000-0003-0795-5320 https://orcid.org/0000-0002-2639-3469 |
url |
https://doi.org/10.3389/fendo.2022.908240 http://hdl.handle.net/1843/60273 https://orcid.org/0000-0001-7587-6662 https://orcid.org/0000-0001-5374-6242 https://orcid.org/0000-0002-9881-1236 https://orcid.org/0000-0002-7209-6043 https://orcid.org/0000-0001-7679-1353 https://orcid.org/0000-0002-5620-6273 https://orcid.org/0000-0003-0795-5320 https://orcid.org/0000-0002-2639-3469 |
identifier_str_mv |
1664-2392 |
dc.language.iso.fl_str_mv |
por |
language |
por |
dc.relation.ispartof.pt_BR.fl_str_mv |
Frontiers in endocrinology |
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info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
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application/pdf |
dc.publisher.none.fl_str_mv |
Universidade Federal de Minas Gerais |
dc.publisher.initials.fl_str_mv |
UFMG |
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Brasil |
dc.publisher.department.fl_str_mv |
ICB - DEPARTAMENTO DE FISIOLOGIA E BIOFÍSICA VET - DEPARTAMENTO DE CLÍNICA E CIRURGIA |
publisher.none.fl_str_mv |
Universidade Federal de Minas Gerais |
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reponame:Repositório Institucional da UFMG instname:Universidade Federal de Minas Gerais (UFMG) instacron:UFMG |
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Universidade Federal de Minas Gerais (UFMG) |
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UFMG |
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