A role for the endocannabinoid system in premature luteal regression and progesterone withdrawal in lipopolysaccharide-induced early pregnancy loss model

Autores
Schander, Julieta Aylen; Correa, Fernando Gabriel; Bariani, Maria Victoria; Blanco, Julieta; Cymeryng, Cora Betriz; Jensen, Cristian Federico; Wolfson, Manuel Luis; Franchi, Ana Maria
Año de publicación
2016
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Appropriate systemic progesterone levels are critical for a successful pregnancy outcome. Precocious loss of luteal progesterone secretion leads to miscarriage in rodents. We have previously shown that lipopolysaccharide (LPS) administration to pregnant mice induces embryonic resorption accompanied by a dramatic decrease in systemic progesterone levels in a murine model of inflammatory miscarriage. Furthermore, we showed that the endocannabinoid system (eCS) mediated LPS deleterious effects. The aim of this study was to explore the participation of the endocrine system in the LPS-induced miscarriage as well as the role of the eCS in this process. We found that LPS increased the expression of COX-2 and the production of PGF2α in the uterus of 7-days pregnant mice. Increased production of PGF2α resulted in a lower expression of prolactin receptor in the ovary and a marked regression of corpora lutea (CL), which thus produces less progesterone and consequently, results in embryo resorption. Remarkably, these effects were completely absent in CB1-knockout pregnant mice. Our results clearly suggest that the absence of CB1 receptor confers resistance to LPS deleterious actions during pregnancy. Moreover, lack of CB1 receptor protected from LPS-induced premature luteal regression.
Fil: Schander, Julieta Aylen. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Fil: Correa, Fernando Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Fil: Bariani, Maria Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Fil: Blanco, Julieta. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Fil: Cymeryng, Cora Betriz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina; Argentina
Fil: Jensen, Cristian Federico. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina; Argentina
Fil: Wolfson, Manuel Luis. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Fil: Franchi, Ana Maria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Materia
Luteolysis
Endocannabinoid System
Cox-2
Pgf2a
Prolactin Receptor
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:11336/47362

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spelling A role for the endocannabinoid system in premature luteal regression and progesterone withdrawal in lipopolysaccharide-induced early pregnancy loss modelSchander, Julieta AylenCorrea, Fernando GabrielBariani, Maria VictoriaBlanco, JulietaCymeryng, Cora BetrizJensen, Cristian FedericoWolfson, Manuel LuisFranchi, Ana MariaLuteolysisEndocannabinoid SystemCox-2Pgf2aProlactin Receptorhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Appropriate systemic progesterone levels are critical for a successful pregnancy outcome. Precocious loss of luteal progesterone secretion leads to miscarriage in rodents. We have previously shown that lipopolysaccharide (LPS) administration to pregnant mice induces embryonic resorption accompanied by a dramatic decrease in systemic progesterone levels in a murine model of inflammatory miscarriage. Furthermore, we showed that the endocannabinoid system (eCS) mediated LPS deleterious effects. The aim of this study was to explore the participation of the endocrine system in the LPS-induced miscarriage as well as the role of the eCS in this process. We found that LPS increased the expression of COX-2 and the production of PGF2α in the uterus of 7-days pregnant mice. Increased production of PGF2α resulted in a lower expression of prolactin receptor in the ovary and a marked regression of corpora lutea (CL), which thus produces less progesterone and consequently, results in embryo resorption. Remarkably, these effects were completely absent in CB1-knockout pregnant mice. Our results clearly suggest that the absence of CB1 receptor confers resistance to LPS deleterious actions during pregnancy. Moreover, lack of CB1 receptor protected from LPS-induced premature luteal regression.Fil: Schander, Julieta Aylen. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; ArgentinaFil: Correa, Fernando Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; ArgentinaFil: Bariani, Maria Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; ArgentinaFil: Blanco, Julieta. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; ArgentinaFil: Cymeryng, Cora Betriz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina; ArgentinaFil: Jensen, Cristian Federico. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina; ArgentinaFil: Wolfson, Manuel Luis. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; ArgentinaFil: Franchi, Ana Maria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; ArgentinaOxford University Press2016-11info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/47362Schander, Julieta Aylen; Correa, Fernando Gabriel; Bariani, Maria Victoria; Blanco, Julieta; Cymeryng, Cora Betriz; et al.; A role for the endocannabinoid system in premature luteal regression and progesterone withdrawal in lipopolysaccharide-induced early pregnancy loss model; Oxford University Press; Molecular Human Reproduction; 22; 11; 11-2016; 800-8081360-9947CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1093/molehr/gaw050info:eu-repo/semantics/altIdentifier/url/https://academic.oup.com/molehr/article/22/11/800/2418643info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:57:22Zoai:ri.conicet.gov.ar:11336/47362instacron: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:34982025-09-03 09:57:22.509CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv A role for the endocannabinoid system in premature luteal regression and progesterone withdrawal in lipopolysaccharide-induced early pregnancy loss model
title A role for the endocannabinoid system in premature luteal regression and progesterone withdrawal in lipopolysaccharide-induced early pregnancy loss model
spellingShingle A role for the endocannabinoid system in premature luteal regression and progesterone withdrawal in lipopolysaccharide-induced early pregnancy loss model
Schander, Julieta Aylen
Luteolysis
Endocannabinoid System
Cox-2
Pgf2a
Prolactin Receptor
title_short A role for the endocannabinoid system in premature luteal regression and progesterone withdrawal in lipopolysaccharide-induced early pregnancy loss model
title_full A role for the endocannabinoid system in premature luteal regression and progesterone withdrawal in lipopolysaccharide-induced early pregnancy loss model
title_fullStr A role for the endocannabinoid system in premature luteal regression and progesterone withdrawal in lipopolysaccharide-induced early pregnancy loss model
title_full_unstemmed A role for the endocannabinoid system in premature luteal regression and progesterone withdrawal in lipopolysaccharide-induced early pregnancy loss model
title_sort A role for the endocannabinoid system in premature luteal regression and progesterone withdrawal in lipopolysaccharide-induced early pregnancy loss model
dc.creator.none.fl_str_mv Schander, Julieta Aylen
Correa, Fernando Gabriel
Bariani, Maria Victoria
Blanco, Julieta
Cymeryng, Cora Betriz
Jensen, Cristian Federico
Wolfson, Manuel Luis
Franchi, Ana Maria
author Schander, Julieta Aylen
author_facet Schander, Julieta Aylen
Correa, Fernando Gabriel
Bariani, Maria Victoria
Blanco, Julieta
Cymeryng, Cora Betriz
Jensen, Cristian Federico
Wolfson, Manuel Luis
Franchi, Ana Maria
author_role author
author2 Correa, Fernando Gabriel
Bariani, Maria Victoria
Blanco, Julieta
Cymeryng, Cora Betriz
Jensen, Cristian Federico
Wolfson, Manuel Luis
Franchi, Ana Maria
author2_role author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Luteolysis
Endocannabinoid System
Cox-2
Pgf2a
Prolactin Receptor
topic Luteolysis
Endocannabinoid System
Cox-2
Pgf2a
Prolactin Receptor
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Appropriate systemic progesterone levels are critical for a successful pregnancy outcome. Precocious loss of luteal progesterone secretion leads to miscarriage in rodents. We have previously shown that lipopolysaccharide (LPS) administration to pregnant mice induces embryonic resorption accompanied by a dramatic decrease in systemic progesterone levels in a murine model of inflammatory miscarriage. Furthermore, we showed that the endocannabinoid system (eCS) mediated LPS deleterious effects. The aim of this study was to explore the participation of the endocrine system in the LPS-induced miscarriage as well as the role of the eCS in this process. We found that LPS increased the expression of COX-2 and the production of PGF2α in the uterus of 7-days pregnant mice. Increased production of PGF2α resulted in a lower expression of prolactin receptor in the ovary and a marked regression of corpora lutea (CL), which thus produces less progesterone and consequently, results in embryo resorption. Remarkably, these effects were completely absent in CB1-knockout pregnant mice. Our results clearly suggest that the absence of CB1 receptor confers resistance to LPS deleterious actions during pregnancy. Moreover, lack of CB1 receptor protected from LPS-induced premature luteal regression.
Fil: Schander, Julieta Aylen. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Fil: Correa, Fernando Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Fil: Bariani, Maria Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Fil: Blanco, Julieta. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Fil: Cymeryng, Cora Betriz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina; Argentina
Fil: Jensen, Cristian Federico. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina; Argentina
Fil: Wolfson, Manuel Luis. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Fil: Franchi, Ana Maria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
description Appropriate systemic progesterone levels are critical for a successful pregnancy outcome. Precocious loss of luteal progesterone secretion leads to miscarriage in rodents. We have previously shown that lipopolysaccharide (LPS) administration to pregnant mice induces embryonic resorption accompanied by a dramatic decrease in systemic progesterone levels in a murine model of inflammatory miscarriage. Furthermore, we showed that the endocannabinoid system (eCS) mediated LPS deleterious effects. The aim of this study was to explore the participation of the endocrine system in the LPS-induced miscarriage as well as the role of the eCS in this process. We found that LPS increased the expression of COX-2 and the production of PGF2α in the uterus of 7-days pregnant mice. Increased production of PGF2α resulted in a lower expression of prolactin receptor in the ovary and a marked regression of corpora lutea (CL), which thus produces less progesterone and consequently, results in embryo resorption. Remarkably, these effects were completely absent in CB1-knockout pregnant mice. Our results clearly suggest that the absence of CB1 receptor confers resistance to LPS deleterious actions during pregnancy. Moreover, lack of CB1 receptor protected from LPS-induced premature luteal regression.
publishDate 2016
dc.date.none.fl_str_mv 2016-11
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/11336/47362
Schander, Julieta Aylen; Correa, Fernando Gabriel; Bariani, Maria Victoria; Blanco, Julieta; Cymeryng, Cora Betriz; et al.; A role for the endocannabinoid system in premature luteal regression and progesterone withdrawal in lipopolysaccharide-induced early pregnancy loss model; Oxford University Press; Molecular Human Reproduction; 22; 11; 11-2016; 800-808
1360-9947
CONICET Digital
CONICET
url http://hdl.handle.net/11336/47362
identifier_str_mv Schander, Julieta Aylen; Correa, Fernando Gabriel; Bariani, Maria Victoria; Blanco, Julieta; Cymeryng, Cora Betriz; et al.; A role for the endocannabinoid system in premature luteal regression and progesterone withdrawal in lipopolysaccharide-induced early pregnancy loss model; Oxford University Press; Molecular Human Reproduction; 22; 11; 11-2016; 800-808
1360-9947
CONICET Digital
CONICET
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language eng
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dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
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eu_rights_str_mv openAccess
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dc.publisher.none.fl_str_mv Oxford University Press
publisher.none.fl_str_mv Oxford University Press
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
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instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
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