Leptin receptor activation increases Sam68 tyrosine phosphorylation and expression in human trophoblastic cells

Autores
Sánchez Jiménez, Flora; Pérez Pérez, Antonio; González Yanes, Carmen; Najib, Souad; Varone, Cecilia Laura; Sánchez Margalet, Víctor
Año de publicación
2011
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Leptin is produced in placenta where it has been found to be an important autocrine signal for trophoblastic growth during pregnancy, promoting antiapoptotic and trophic effects. Leptin receptor is present in trophoblastic cells and leptin may fully activate signaling. We have previously implicated the RNA-binding protein Sam68 in leptin signal transduction in immune cells. In the present work, we have studied the possible role of Sam68 in leptin receptor signaling in trophoblastic cells (JEG-3 cells). Leptin dose-dependently stimulated Sam68 phosphorylation in JEG-3 cells, as assessed by immunoprecipitation and immunoblot with anti-phosphotyrosine antibodies. As previously observed in other systems, tyrosine phosphorylation of Sam68 in response to leptin inhibits its RNA binding capacity. Besides, leptin stimulation dose-dependently increases Sam68 expression in JEG-3 cells, as assessed by quantitative PCR. Consistently, the amount of Sam68 protein is increased after 24. h of leptin stimulation of trophoblastic cells. In order to study the possible role of Sam68 on leptin receptor synthesis, we employed antisense strategy to knockdown the expression of Sam68. We have found that a decrease in Sam68 expression leads to a decrease in leptin receptor amount in JEG-3 cells, as assessed both by quantitative PCR and immunoblot.These results strongly suggest the participation of Sam68 in leptin receptor signaling in human trophoblastic cells, and therefore, Sam68 may mediate some of the leptin effects in placenta.
Fil: Sánchez Jiménez, Flora. Hospital Universitario Virgen Macarena; España
Fil: Pérez Pérez, Antonio. Hospital Universitario Virgen Macarena; España
Fil: González Yanes, Carmen. Hospital Universitario Virgen Macarena; España
Fil: Najib, Souad. Institut de Médecine Moléculaire de Rangueil; Francia
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
Fil: Sánchez Margalet, Víctor. Hospital Universitario Virgen Macarena; España
Materia
LEPTIN RECEPTOR
PLACENTA
SAM68
SIGNAL TRANSDUCTION
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:11336/95881
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/95881
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Leptin receptor activation increases Sam68 tyrosine phosphorylation and expression in human trophoblastic cellsSánchez Jiménez, FloraPérez Pérez, AntonioGonzález Yanes, CarmenNajib, SouadVarone, Cecilia LauraSánchez Margalet, VíctorLEPTIN RECEPTORPLACENTASAM68SIGNAL TRANSDUCTIONhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Leptin is produced in placenta where it has been found to be an important autocrine signal for trophoblastic growth during pregnancy, promoting antiapoptotic and trophic effects. Leptin receptor is present in trophoblastic cells and leptin may fully activate signaling. We have previously implicated the RNA-binding protein Sam68 in leptin signal transduction in immune cells. In the present work, we have studied the possible role of Sam68 in leptin receptor signaling in trophoblastic cells (JEG-3 cells). Leptin dose-dependently stimulated Sam68 phosphorylation in JEG-3 cells, as assessed by immunoprecipitation and immunoblot with anti-phosphotyrosine antibodies. As previously observed in other systems, tyrosine phosphorylation of Sam68 in response to leptin inhibits its RNA binding capacity. Besides, leptin stimulation dose-dependently increases Sam68 expression in JEG-3 cells, as assessed by quantitative PCR. Consistently, the amount of Sam68 protein is increased after 24. h of leptin stimulation of trophoblastic cells. In order to study the possible role of Sam68 on leptin receptor synthesis, we employed antisense strategy to knockdown the expression of Sam68. We have found that a decrease in Sam68 expression leads to a decrease in leptin receptor amount in JEG-3 cells, as assessed both by quantitative PCR and immunoblot.These results strongly suggest the participation of Sam68 in leptin receptor signaling in human trophoblastic cells, and therefore, Sam68 may mediate some of the leptin effects in placenta.Fil: Sánchez Jiménez, Flora. Hospital Universitario Virgen Macarena; EspañaFil: Pérez Pérez, Antonio. Hospital Universitario Virgen Macarena; EspañaFil: González Yanes, Carmen. Hospital Universitario Virgen Macarena; EspañaFil: Najib, Souad. Institut de Médecine Moléculaire de Rangueil; FranciaFil: 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; ArgentinaFil: Sánchez Margalet, Víctor. Hospital Universitario Virgen Macarena; EspañaElsevier Ireland2011-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/95881Sánchez Jiménez, Flora; Pérez Pérez, Antonio; González Yanes, Carmen; Najib, Souad; Varone, Cecilia Laura; et al.; Leptin receptor activation increases Sam68 tyrosine phosphorylation and expression in human trophoblastic cells; Elsevier Ireland; Molecular and Cellular Endocrinology; 332; 1-2; 1-2011; 221-2270303-7207CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0303720710005022info:eu-repo/semantics/altIdentifier/doi/10.1016/j.mce.2010.10.014info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:38:05Zoai:ri.conicet.gov.ar:11336/95881instacron: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 10:38:06.023CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Leptin receptor activation increases Sam68 tyrosine phosphorylation and expression in human trophoblastic cells
title Leptin receptor activation increases Sam68 tyrosine phosphorylation and expression in human trophoblastic cells
spellingShingle Leptin receptor activation increases Sam68 tyrosine phosphorylation and expression in human trophoblastic cells
Sánchez Jiménez, Flora
LEPTIN RECEPTOR
PLACENTA
SAM68
SIGNAL TRANSDUCTION
title_short Leptin receptor activation increases Sam68 tyrosine phosphorylation and expression in human trophoblastic cells
title_full Leptin receptor activation increases Sam68 tyrosine phosphorylation and expression in human trophoblastic cells
title_fullStr Leptin receptor activation increases Sam68 tyrosine phosphorylation and expression in human trophoblastic cells
title_full_unstemmed Leptin receptor activation increases Sam68 tyrosine phosphorylation and expression in human trophoblastic cells
title_sort Leptin receptor activation increases Sam68 tyrosine phosphorylation and expression in human trophoblastic cells
dc.creator.none.fl_str_mv Sánchez Jiménez, Flora
Pérez Pérez, Antonio
González Yanes, Carmen
Najib, Souad
Varone, Cecilia Laura
Sánchez Margalet, Víctor
author Sánchez Jiménez, Flora
author_facet Sánchez Jiménez, Flora
Pérez Pérez, Antonio
González Yanes, Carmen
Najib, Souad
Varone, Cecilia Laura
Sánchez Margalet, Víctor
author_role author
author2 Pérez Pérez, Antonio
González Yanes, Carmen
Najib, Souad
Varone, Cecilia Laura
Sánchez Margalet, Víctor
author2_role author
author
author
author
author
dc.subject.none.fl_str_mv LEPTIN RECEPTOR
PLACENTA
SAM68
SIGNAL TRANSDUCTION
topic LEPTIN RECEPTOR
PLACENTA
SAM68
SIGNAL TRANSDUCTION
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Leptin is produced in placenta where it has been found to be an important autocrine signal for trophoblastic growth during pregnancy, promoting antiapoptotic and trophic effects. Leptin receptor is present in trophoblastic cells and leptin may fully activate signaling. We have previously implicated the RNA-binding protein Sam68 in leptin signal transduction in immune cells. In the present work, we have studied the possible role of Sam68 in leptin receptor signaling in trophoblastic cells (JEG-3 cells). Leptin dose-dependently stimulated Sam68 phosphorylation in JEG-3 cells, as assessed by immunoprecipitation and immunoblot with anti-phosphotyrosine antibodies. As previously observed in other systems, tyrosine phosphorylation of Sam68 in response to leptin inhibits its RNA binding capacity. Besides, leptin stimulation dose-dependently increases Sam68 expression in JEG-3 cells, as assessed by quantitative PCR. Consistently, the amount of Sam68 protein is increased after 24. h of leptin stimulation of trophoblastic cells. In order to study the possible role of Sam68 on leptin receptor synthesis, we employed antisense strategy to knockdown the expression of Sam68. We have found that a decrease in Sam68 expression leads to a decrease in leptin receptor amount in JEG-3 cells, as assessed both by quantitative PCR and immunoblot.These results strongly suggest the participation of Sam68 in leptin receptor signaling in human trophoblastic cells, and therefore, Sam68 may mediate some of the leptin effects in placenta.
Fil: Sánchez Jiménez, Flora. Hospital Universitario Virgen Macarena; España
Fil: Pérez Pérez, Antonio. Hospital Universitario Virgen Macarena; España
Fil: González Yanes, Carmen. Hospital Universitario Virgen Macarena; España
Fil: Najib, Souad. Institut de Médecine Moléculaire de Rangueil; Francia
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
Fil: Sánchez Margalet, Víctor. Hospital Universitario Virgen Macarena; España
description Leptin is produced in placenta where it has been found to be an important autocrine signal for trophoblastic growth during pregnancy, promoting antiapoptotic and trophic effects. Leptin receptor is present in trophoblastic cells and leptin may fully activate signaling. We have previously implicated the RNA-binding protein Sam68 in leptin signal transduction in immune cells. In the present work, we have studied the possible role of Sam68 in leptin receptor signaling in trophoblastic cells (JEG-3 cells). Leptin dose-dependently stimulated Sam68 phosphorylation in JEG-3 cells, as assessed by immunoprecipitation and immunoblot with anti-phosphotyrosine antibodies. As previously observed in other systems, tyrosine phosphorylation of Sam68 in response to leptin inhibits its RNA binding capacity. Besides, leptin stimulation dose-dependently increases Sam68 expression in JEG-3 cells, as assessed by quantitative PCR. Consistently, the amount of Sam68 protein is increased after 24. h of leptin stimulation of trophoblastic cells. In order to study the possible role of Sam68 on leptin receptor synthesis, we employed antisense strategy to knockdown the expression of Sam68. We have found that a decrease in Sam68 expression leads to a decrease in leptin receptor amount in JEG-3 cells, as assessed both by quantitative PCR and immunoblot.These results strongly suggest the participation of Sam68 in leptin receptor signaling in human trophoblastic cells, and therefore, Sam68 may mediate some of the leptin effects in placenta.
publishDate 2011
dc.date.none.fl_str_mv 2011-01
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/95881
Sánchez Jiménez, Flora; Pérez Pérez, Antonio; González Yanes, Carmen; Najib, Souad; Varone, Cecilia Laura; et al.; Leptin receptor activation increases Sam68 tyrosine phosphorylation and expression in human trophoblastic cells; Elsevier Ireland; Molecular and Cellular Endocrinology; 332; 1-2; 1-2011; 221-227
0303-7207
CONICET Digital
CONICET
url http://hdl.handle.net/11336/95881
identifier_str_mv Sánchez Jiménez, Flora; Pérez Pérez, Antonio; González Yanes, Carmen; Najib, Souad; Varone, Cecilia Laura; et al.; Leptin receptor activation increases Sam68 tyrosine phosphorylation and expression in human trophoblastic cells; Elsevier Ireland; Molecular and Cellular Endocrinology; 332; 1-2; 1-2011; 221-227
0303-7207
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/pii/S0303720710005022
info:eu-repo/semantics/altIdentifier/doi/10.1016/j.mce.2010.10.014
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
dc.publisher.none.fl_str_mv Elsevier Ireland
publisher.none.fl_str_mv Elsevier Ireland
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
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score 13.070432

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