Crosstalk between ERα and NFκB transcription factors on E2 induced leptin expression in placental cells

Autores
Shanton, Malena; Camisay, Maria Fernanda; Pérez Pérez, Antonio; Maskin, Bernardo; Casale, Roberto; Sánchez Margalet, Victor; Erlejman, Alejandra Giselle; Varone, Cecilia Laura
Año de publicación
2019
Idioma
inglés
Tipo de recurso
documento de conferencia
Estado
versión publicada
Descripción
Objectives: Leptin is a key hormone in placental physiology. It regulates trophoblast proliferation, inhibits apoptosis, stimulates protein synthesis, and regulates fetal growth and development. It plays an important role in reproduction mainly because it has been suggested to have function in the placenta during the gestation, where leptin and leptin receptors expression were detected. Previous results from our lab demonstrated that estradiol (E2) regulates leptin expression involving genomic and nongenomic effects. In the present work, we analysed the crosstalk between estrogen receptor alpha (ERa) and NFkB transcription factors on E2 induced leptin expression in human trophoblast cells. Methods: BeWo cells, cultured and human term placental explants were used. Western blot, immunocytochemistry, co-immunoprecipitation and transfection assays were carried out. Ethical review committee at the Alejandro Posadas National Hospital approved all procedures. Results: We found that E2 treatment significantly enhanced the NFkB member p65 expression both in BeWo cells and human term placental explants. Moreover E2 increased IkBa phosphorylation and NFkB transcriptional activity determined by reporter analysis. We also evaluated the localization of ERa and p65 NFkB subunit in BeWo cells by immunofluorescence assay. We found that both proteins are located in the cytoplasm and migrate to the nucleus when they are overexpressed. Besides ERa and p65 form a complex determined by co-immunoprecipitation, as previously seen. These findings suggest that the transcription factor NFkB, might be affecting estradiol leptin induction. Finally through transient transfection analysis we observed that the overexpression of RelA (p65) and HEGO (ERa) increases basal transcriptional activity of leptin promoter. Conclusion: These results suggest that leptin expression is tightly regulated and help to comprehend the mechanisms where E2 regulated leptin expression possibly involving the cooperation between ERa and NFkB transcription factors.
Fil: Shanton, Malena. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; Argentina
Fil: Camisay, Maria Fernanda. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; Argentina
Fil: Pérez Pérez, Antonio. Universidad de Sevilla; España
Fil: Maskin, Bernardo. Hospital Nacional Profesor Alejandro Posadas; Argentina
Fil: Casale, Roberto. Hospital Nacional Profesor Alejandro Posadas; Argentina
Fil: Sánchez Margalet, Victor. Universidad de Sevilla; España
Fil: Erlejman, Alejandra Giselle. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; Argentina
Fil: Varone, Cecilia Laura. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; Argentina
International Federation of Placenta Associations Meeting y VIII Simposio Latinoamericano de Interacción Materno-Fetal y Placenta
Buenos Aires
Argentina
International Federation of Placenta Associations
Materia
Leptin
NFkB
ERalfa
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/135669
Acceder
id CONICETDig_2c03b3165311f776e3b314a1e18dce2c
oai_identifier_str oai:ri.conicet.gov.ar:11336/135669
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Crosstalk between ERα and NFκB transcription factors on E2 induced leptin expression in placental cellsShanton, MalenaCamisay, Maria FernandaPérez Pérez, AntonioMaskin, BernardoCasale, RobertoSánchez Margalet, VictorErlejman, Alejandra GiselleVarone, Cecilia LauraLeptinNFkBERalfahttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Objectives: Leptin is a key hormone in placental physiology. It regulates trophoblast proliferation, inhibits apoptosis, stimulates protein synthesis, and regulates fetal growth and development. It plays an important role in reproduction mainly because it has been suggested to have function in the placenta during the gestation, where leptin and leptin receptors expression were detected. Previous results from our lab demonstrated that estradiol (E2) regulates leptin expression involving genomic and nongenomic effects. In the present work, we analysed the crosstalk between estrogen receptor alpha (ERa) and NFkB transcription factors on E2 induced leptin expression in human trophoblast cells. Methods: BeWo cells, cultured and human term placental explants were used. Western blot, immunocytochemistry, co-immunoprecipitation and transfection assays were carried out. Ethical review committee at the Alejandro Posadas National Hospital approved all procedures. Results: We found that E2 treatment significantly enhanced the NFkB member p65 expression both in BeWo cells and human term placental explants. Moreover E2 increased IkBa phosphorylation and NFkB transcriptional activity determined by reporter analysis. We also evaluated the localization of ERa and p65 NFkB subunit in BeWo cells by immunofluorescence assay. We found that both proteins are located in the cytoplasm and migrate to the nucleus when they are overexpressed. Besides ERa and p65 form a complex determined by co-immunoprecipitation, as previously seen. These findings suggest that the transcription factor NFkB, might be affecting estradiol leptin induction. Finally through transient transfection analysis we observed that the overexpression of RelA (p65) and HEGO (ERa) increases basal transcriptional activity of leptin promoter. Conclusion: These results suggest that leptin expression is tightly regulated and help to comprehend the mechanisms where E2 regulated leptin expression possibly involving the cooperation between ERa and NFkB transcription factors.Fil: Shanton, Malena. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; ArgentinaFil: Camisay, Maria Fernanda. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; ArgentinaFil: Pérez Pérez, Antonio. Universidad de Sevilla; EspañaFil: Maskin, Bernardo. Hospital Nacional Profesor Alejandro Posadas; ArgentinaFil: Casale, Roberto. Hospital Nacional Profesor Alejandro Posadas; ArgentinaFil: Sánchez Margalet, Victor. Universidad de Sevilla; EspañaFil: Erlejman, Alejandra Giselle. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; ArgentinaFil: Varone, Cecilia Laura. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; ArgentinaInternational Federation of Placenta Associations Meeting y VIII Simposio Latinoamericano de Interacción Materno-Fetal y PlacentaBuenos AiresArgentinaInternational Federation of Placenta AssociationsElsevier2019info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/conferenceObjectReuniónJournalhttp://purl.org/coar/resource_type/c_5794info:ar-repo/semantics/documentoDeConferenciaapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/135669Crosstalk between ERα and NFκB transcription factors on E2 induced leptin expression in placental cells; International Federation of Placenta Associations Meeting y VIII Simposio Latinoamericano de Interacción Materno-Fetal y Placenta; Buenos Aires; Argentina; 2019; e33-e330143-4004CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/abs/pii/S0143400419302383info:eu-repo/semantics/altIdentifier/doi/10.1016/j.placenta.2019.06.109Internacionalinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:39:13Zoai:ri.conicet.gov.ar:11336/135669instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-29 10:39:13.996CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Crosstalk between ERα and NFκB transcription factors on E2 induced leptin expression in placental cells
title Crosstalk between ERα and NFκB transcription factors on E2 induced leptin expression in placental cells
spellingShingle Crosstalk between ERα and NFκB transcription factors on E2 induced leptin expression in placental cells
Shanton, Malena
Leptin
NFkB
ERalfa
title_short Crosstalk between ERα and NFκB transcription factors on E2 induced leptin expression in placental cells
title_full Crosstalk between ERα and NFκB transcription factors on E2 induced leptin expression in placental cells
title_fullStr Crosstalk between ERα and NFκB transcription factors on E2 induced leptin expression in placental cells
title_full_unstemmed Crosstalk between ERα and NFκB transcription factors on E2 induced leptin expression in placental cells
title_sort Crosstalk between ERα and NFκB transcription factors on E2 induced leptin expression in placental cells
dc.creator.none.fl_str_mv Shanton, Malena
Camisay, Maria Fernanda
Pérez Pérez, Antonio
Maskin, Bernardo
Casale, Roberto
Sánchez Margalet, Victor
Erlejman, Alejandra Giselle
Varone, Cecilia Laura
author Shanton, Malena
author_facet Shanton, Malena
Camisay, Maria Fernanda
Pérez Pérez, Antonio
Maskin, Bernardo
Casale, Roberto
Sánchez Margalet, Victor
Erlejman, Alejandra Giselle
Varone, Cecilia Laura
author_role author
author2 Camisay, Maria Fernanda
Pérez Pérez, Antonio
Maskin, Bernardo
Casale, Roberto
Sánchez Margalet, Victor
Erlejman, Alejandra Giselle
Varone, Cecilia Laura
author2_role author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Leptin
NFkB
ERalfa
topic Leptin
NFkB
ERalfa
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Objectives: Leptin is a key hormone in placental physiology. It regulates trophoblast proliferation, inhibits apoptosis, stimulates protein synthesis, and regulates fetal growth and development. It plays an important role in reproduction mainly because it has been suggested to have function in the placenta during the gestation, where leptin and leptin receptors expression were detected. Previous results from our lab demonstrated that estradiol (E2) regulates leptin expression involving genomic and nongenomic effects. In the present work, we analysed the crosstalk between estrogen receptor alpha (ERa) and NFkB transcription factors on E2 induced leptin expression in human trophoblast cells. Methods: BeWo cells, cultured and human term placental explants were used. Western blot, immunocytochemistry, co-immunoprecipitation and transfection assays were carried out. Ethical review committee at the Alejandro Posadas National Hospital approved all procedures. Results: We found that E2 treatment significantly enhanced the NFkB member p65 expression both in BeWo cells and human term placental explants. Moreover E2 increased IkBa phosphorylation and NFkB transcriptional activity determined by reporter analysis. We also evaluated the localization of ERa and p65 NFkB subunit in BeWo cells by immunofluorescence assay. We found that both proteins are located in the cytoplasm and migrate to the nucleus when they are overexpressed. Besides ERa and p65 form a complex determined by co-immunoprecipitation, as previously seen. These findings suggest that the transcription factor NFkB, might be affecting estradiol leptin induction. Finally through transient transfection analysis we observed that the overexpression of RelA (p65) and HEGO (ERa) increases basal transcriptional activity of leptin promoter. Conclusion: These results suggest that leptin expression is tightly regulated and help to comprehend the mechanisms where E2 regulated leptin expression possibly involving the cooperation between ERa and NFkB transcription factors.
Fil: Shanton, Malena. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; Argentina
Fil: Camisay, Maria Fernanda. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; Argentina
Fil: Pérez Pérez, Antonio. Universidad de Sevilla; España
Fil: Maskin, Bernardo. Hospital Nacional Profesor Alejandro Posadas; Argentina
Fil: Casale, Roberto. Hospital Nacional Profesor Alejandro Posadas; Argentina
Fil: Sánchez Margalet, Victor. Universidad de Sevilla; España
Fil: Erlejman, Alejandra Giselle. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; Argentina
Fil: Varone, Cecilia Laura. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; Argentina
International Federation of Placenta Associations Meeting y VIII Simposio Latinoamericano de Interacción Materno-Fetal y Placenta
Buenos Aires
Argentina
International Federation of Placenta Associations
description Objectives: Leptin is a key hormone in placental physiology. It regulates trophoblast proliferation, inhibits apoptosis, stimulates protein synthesis, and regulates fetal growth and development. It plays an important role in reproduction mainly because it has been suggested to have function in the placenta during the gestation, where leptin and leptin receptors expression were detected. Previous results from our lab demonstrated that estradiol (E2) regulates leptin expression involving genomic and nongenomic effects. In the present work, we analysed the crosstalk between estrogen receptor alpha (ERa) and NFkB transcription factors on E2 induced leptin expression in human trophoblast cells. Methods: BeWo cells, cultured and human term placental explants were used. Western blot, immunocytochemistry, co-immunoprecipitation and transfection assays were carried out. Ethical review committee at the Alejandro Posadas National Hospital approved all procedures. Results: We found that E2 treatment significantly enhanced the NFkB member p65 expression both in BeWo cells and human term placental explants. Moreover E2 increased IkBa phosphorylation and NFkB transcriptional activity determined by reporter analysis. We also evaluated the localization of ERa and p65 NFkB subunit in BeWo cells by immunofluorescence assay. We found that both proteins are located in the cytoplasm and migrate to the nucleus when they are overexpressed. Besides ERa and p65 form a complex determined by co-immunoprecipitation, as previously seen. These findings suggest that the transcription factor NFkB, might be affecting estradiol leptin induction. Finally through transient transfection analysis we observed that the overexpression of RelA (p65) and HEGO (ERa) increases basal transcriptional activity of leptin promoter. Conclusion: These results suggest that leptin expression is tightly regulated and help to comprehend the mechanisms where E2 regulated leptin expression possibly involving the cooperation between ERa and NFkB transcription factors.
publishDate 2019
dc.date.none.fl_str_mv 2019
dc.type.none.fl_str_mv info:eu-repo/semantics/publishedVersion
info:eu-repo/semantics/conferenceObject
Reunión
Journal
http://purl.org/coar/resource_type/c_5794
info:ar-repo/semantics/documentoDeConferencia
status_str publishedVersion
format conferenceObject
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/135669
Crosstalk between ERα and NFκB transcription factors on E2 induced leptin expression in placental cells; International Federation of Placenta Associations Meeting y VIII Simposio Latinoamericano de Interacción Materno-Fetal y Placenta; Buenos Aires; Argentina; 2019; e33-e33
0143-4004
CONICET Digital
CONICET
url http://hdl.handle.net/11336/135669
identifier_str_mv Crosstalk between ERα and NFκB transcription factors on E2 induced leptin expression in placental cells; International Federation of Placenta Associations Meeting y VIII Simposio Latinoamericano de Interacción Materno-Fetal y Placenta; Buenos Aires; Argentina; 2019; e33-e33
0143-4004
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/abs/pii/S0143400419302383
info:eu-repo/semantics/altIdentifier/doi/10.1016/j.placenta.2019.06.109
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
dc.coverage.none.fl_str_mv Internacional
dc.publisher.none.fl_str_mv Elsevier
publisher.none.fl_str_mv Elsevier
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
_version_ 1844614417289838592
score 13.070432

Publicaciones similares