17β-oestradiol acts as a negative modulator of insulin-induced lactotroph cell proliferation through oestrogen receptor alpha, via nitric oxide/guanylyl cyclase/cGMP

Autores
Gutierrez, Silvina Gabriela; Petiti, Juan Pablo; Sosa, Liliana del Valle; Fozzatti, Laura; de Paul, Ana Lucia; Masini, Ana María; Torres, Alicia Ines
Año de publicación
2010
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Objectives: 17b-oestradiol interacts with growth factors to modulate lactotroph cell population. However, contribution of isoforms of the oestrogen receptor in these activities is not fully understood. In the present study, we have established participation of a and b oestrogen receptors in effects of 17b-oestradiol on lactotroph proliferation induced by insulin and shown involvement of the NO⁄sGC⁄ cGMP pathway. Materials and methods: Cell cultures were prepared from anterior pituitaries of female rats to evaluate lactotroph cell proliferation using bromodeoxyuridine (BrdUrd) detection, protein expression by western blotting and cGMP by enzyme immunoassay. Results: In serum-free conditions, 17b-oestradiol and a and b oestrogen receptor agonists (PPT and DPN) failed to increase numbers of lactotroph cells undergoing mitosis. Co-incubation of 17b-oestradiol⁄insulin and PPT⁄insulin significantly decreased lactotroph mitogenic activity promoted by insulin alone. Both ICI 182780 and NOS inhibitors (L-NMMA and L-NAME) induced reversal of the anti-proliferative effect promoted by 17b-oestradiol⁄ insulin and PPT⁄insulin. Moreover, 17b-oestradiol, PPT and insulin increased sGC a1 protein expression and inhibited b1, whereas co-incubation of 17boestradiol⁄insulin or PPT⁄insulin induced increases of the two isoforms a1 and b1. 17b-oestradiol and insulin reduced cGMP production, while 17b-oestradiol⁄insulin co-incubation increased this cyclic nucleotide. Conclusions: Our results suggest that 17b-oestradiol is capable of arresting lactotroph proliferation induced by insulin through ER a with participation of the signalling NO⁄sGC⁄ cGMP pathway
Fil: Gutierrez, Silvina Gabriela. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopía Electrónica; Argentina
Fil: Petiti, Juan Pablo. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopía Electrónica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; Argentina
Fil: Sosa, Liliana del Valle. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopía Electrónica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; Argentina
Fil: Fozzatti, Laura. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: de Paul, Ana Lucia. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopía Electrónica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; Argentina
Fil: Masini, Ana María. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: Torres, Alicia Ines. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopía Electrónica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; Argentina
Materia
Cell Proliferation
Estrogen Receptor alpha
Insulin
Nitric Oxide
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:11336/187838
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/187838
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling 17β-oestradiol acts as a negative modulator of insulin-induced lactotroph cell proliferation through oestrogen receptor alpha, via nitric oxide/guanylyl cyclase/cGMPGutierrez, Silvina GabrielaPetiti, Juan PabloSosa, Liliana del ValleFozzatti, Laurade Paul, Ana LuciaMasini, Ana MaríaTorres, Alicia InesCell ProliferationEstrogen Receptor alphaInsulinNitric Oxidehttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Objectives: 17b-oestradiol interacts with growth factors to modulate lactotroph cell population. However, contribution of isoforms of the oestrogen receptor in these activities is not fully understood. In the present study, we have established participation of a and b oestrogen receptors in effects of 17b-oestradiol on lactotroph proliferation induced by insulin and shown involvement of the NO⁄sGC⁄ cGMP pathway. Materials and methods: Cell cultures were prepared from anterior pituitaries of female rats to evaluate lactotroph cell proliferation using bromodeoxyuridine (BrdUrd) detection, protein expression by western blotting and cGMP by enzyme immunoassay. Results: In serum-free conditions, 17b-oestradiol and a and b oestrogen receptor agonists (PPT and DPN) failed to increase numbers of lactotroph cells undergoing mitosis. Co-incubation of 17b-oestradiol⁄insulin and PPT⁄insulin significantly decreased lactotroph mitogenic activity promoted by insulin alone. Both ICI 182780 and NOS inhibitors (L-NMMA and L-NAME) induced reversal of the anti-proliferative effect promoted by 17b-oestradiol⁄ insulin and PPT⁄insulin. Moreover, 17b-oestradiol, PPT and insulin increased sGC a1 protein expression and inhibited b1, whereas co-incubation of 17boestradiol⁄insulin or PPT⁄insulin induced increases of the two isoforms a1 and b1. 17b-oestradiol and insulin reduced cGMP production, while 17b-oestradiol⁄insulin co-incubation increased this cyclic nucleotide. Conclusions: Our results suggest that 17b-oestradiol is capable of arresting lactotroph proliferation induced by insulin through ER a with participation of the signalling NO⁄sGC⁄ cGMP pathwayFil: Gutierrez, Silvina Gabriela. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopía Electrónica; ArgentinaFil: Petiti, Juan Pablo. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopía Electrónica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; ArgentinaFil: Sosa, Liliana del Valle. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopía Electrónica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; ArgentinaFil: Fozzatti, Laura. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaFil: de Paul, Ana Lucia. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopía Electrónica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; ArgentinaFil: Masini, Ana María. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaFil: Torres, Alicia Ines. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopía Electrónica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; ArgentinaWiley Blackwell Publishing, Inc2010-10info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/187838Gutierrez, Silvina Gabriela; Petiti, Juan Pablo; Sosa, Liliana del Valle; Fozzatti, Laura; de Paul, Ana Lucia; et al.; 17β-oestradiol acts as a negative modulator of insulin-induced lactotroph cell proliferation through oestrogen receptor alpha, via nitric oxide/guanylyl cyclase/cGMP; Wiley Blackwell Publishing, Inc; Cell Proliferation; 43; 5; 10-2010; 505-5140960-77221365-2184CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://onlinelibrary.wiley.com/doi/10.1111/j.1365-2184.2010.00700.xinfo:eu-repo/semantics/altIdentifier/doi/10.1111/j.1365-2184.2010.00700.xinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-22T12:15:44Zoai:ri.conicet.gov.ar:11336/187838instacron: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:34982025-10-22 12:15:44.493CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv 17β-oestradiol acts as a negative modulator of insulin-induced lactotroph cell proliferation through oestrogen receptor alpha, via nitric oxide/guanylyl cyclase/cGMP
title 17β-oestradiol acts as a negative modulator of insulin-induced lactotroph cell proliferation through oestrogen receptor alpha, via nitric oxide/guanylyl cyclase/cGMP
spellingShingle 17β-oestradiol acts as a negative modulator of insulin-induced lactotroph cell proliferation through oestrogen receptor alpha, via nitric oxide/guanylyl cyclase/cGMP
Gutierrez, Silvina Gabriela
Cell Proliferation
Estrogen Receptor alpha
Insulin
Nitric Oxide
title_short 17β-oestradiol acts as a negative modulator of insulin-induced lactotroph cell proliferation through oestrogen receptor alpha, via nitric oxide/guanylyl cyclase/cGMP
title_full 17β-oestradiol acts as a negative modulator of insulin-induced lactotroph cell proliferation through oestrogen receptor alpha, via nitric oxide/guanylyl cyclase/cGMP
title_fullStr 17β-oestradiol acts as a negative modulator of insulin-induced lactotroph cell proliferation through oestrogen receptor alpha, via nitric oxide/guanylyl cyclase/cGMP
title_full_unstemmed 17β-oestradiol acts as a negative modulator of insulin-induced lactotroph cell proliferation through oestrogen receptor alpha, via nitric oxide/guanylyl cyclase/cGMP
title_sort 17β-oestradiol acts as a negative modulator of insulin-induced lactotroph cell proliferation through oestrogen receptor alpha, via nitric oxide/guanylyl cyclase/cGMP
dc.creator.none.fl_str_mv Gutierrez, Silvina Gabriela
Petiti, Juan Pablo
Sosa, Liliana del Valle
Fozzatti, Laura
de Paul, Ana Lucia
Masini, Ana María
Torres, Alicia Ines
author Gutierrez, Silvina Gabriela
author_facet Gutierrez, Silvina Gabriela
Petiti, Juan Pablo
Sosa, Liliana del Valle
Fozzatti, Laura
de Paul, Ana Lucia
Masini, Ana María
Torres, Alicia Ines
author_role author
author2 Petiti, Juan Pablo
Sosa, Liliana del Valle
Fozzatti, Laura
de Paul, Ana Lucia
Masini, Ana María
Torres, Alicia Ines
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv Cell Proliferation
Estrogen Receptor alpha
Insulin
Nitric Oxide
topic Cell Proliferation
Estrogen Receptor alpha
Insulin
Nitric Oxide
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Objectives: 17b-oestradiol interacts with growth factors to modulate lactotroph cell population. However, contribution of isoforms of the oestrogen receptor in these activities is not fully understood. In the present study, we have established participation of a and b oestrogen receptors in effects of 17b-oestradiol on lactotroph proliferation induced by insulin and shown involvement of the NO⁄sGC⁄ cGMP pathway. Materials and methods: Cell cultures were prepared from anterior pituitaries of female rats to evaluate lactotroph cell proliferation using bromodeoxyuridine (BrdUrd) detection, protein expression by western blotting and cGMP by enzyme immunoassay. Results: In serum-free conditions, 17b-oestradiol and a and b oestrogen receptor agonists (PPT and DPN) failed to increase numbers of lactotroph cells undergoing mitosis. Co-incubation of 17b-oestradiol⁄insulin and PPT⁄insulin significantly decreased lactotroph mitogenic activity promoted by insulin alone. Both ICI 182780 and NOS inhibitors (L-NMMA and L-NAME) induced reversal of the anti-proliferative effect promoted by 17b-oestradiol⁄ insulin and PPT⁄insulin. Moreover, 17b-oestradiol, PPT and insulin increased sGC a1 protein expression and inhibited b1, whereas co-incubation of 17boestradiol⁄insulin or PPT⁄insulin induced increases of the two isoforms a1 and b1. 17b-oestradiol and insulin reduced cGMP production, while 17b-oestradiol⁄insulin co-incubation increased this cyclic nucleotide. Conclusions: Our results suggest that 17b-oestradiol is capable of arresting lactotroph proliferation induced by insulin through ER a with participation of the signalling NO⁄sGC⁄ cGMP pathway
Fil: Gutierrez, Silvina Gabriela. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopía Electrónica; Argentina
Fil: Petiti, Juan Pablo. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopía Electrónica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; Argentina
Fil: Sosa, Liliana del Valle. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopía Electrónica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; Argentina
Fil: Fozzatti, Laura. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: de Paul, Ana Lucia. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopía Electrónica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; Argentina
Fil: Masini, Ana María. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: Torres, Alicia Ines. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopía Electrónica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba; Argentina
description Objectives: 17b-oestradiol interacts with growth factors to modulate lactotroph cell population. However, contribution of isoforms of the oestrogen receptor in these activities is not fully understood. In the present study, we have established participation of a and b oestrogen receptors in effects of 17b-oestradiol on lactotroph proliferation induced by insulin and shown involvement of the NO⁄sGC⁄ cGMP pathway. Materials and methods: Cell cultures were prepared from anterior pituitaries of female rats to evaluate lactotroph cell proliferation using bromodeoxyuridine (BrdUrd) detection, protein expression by western blotting and cGMP by enzyme immunoassay. Results: In serum-free conditions, 17b-oestradiol and a and b oestrogen receptor agonists (PPT and DPN) failed to increase numbers of lactotroph cells undergoing mitosis. Co-incubation of 17b-oestradiol⁄insulin and PPT⁄insulin significantly decreased lactotroph mitogenic activity promoted by insulin alone. Both ICI 182780 and NOS inhibitors (L-NMMA and L-NAME) induced reversal of the anti-proliferative effect promoted by 17b-oestradiol⁄ insulin and PPT⁄insulin. Moreover, 17b-oestradiol, PPT and insulin increased sGC a1 protein expression and inhibited b1, whereas co-incubation of 17boestradiol⁄insulin or PPT⁄insulin induced increases of the two isoforms a1 and b1. 17b-oestradiol and insulin reduced cGMP production, while 17b-oestradiol⁄insulin co-incubation increased this cyclic nucleotide. Conclusions: Our results suggest that 17b-oestradiol is capable of arresting lactotroph proliferation induced by insulin through ER a with participation of the signalling NO⁄sGC⁄ cGMP pathway
publishDate 2010
dc.date.none.fl_str_mv 2010-10
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/11336/187838
Gutierrez, Silvina Gabriela; Petiti, Juan Pablo; Sosa, Liliana del Valle; Fozzatti, Laura; de Paul, Ana Lucia; et al.; 17β-oestradiol acts as a negative modulator of insulin-induced lactotroph cell proliferation through oestrogen receptor alpha, via nitric oxide/guanylyl cyclase/cGMP; Wiley Blackwell Publishing, Inc; Cell Proliferation; 43; 5; 10-2010; 505-514
0960-7722
1365-2184
CONICET Digital
CONICET
url http://hdl.handle.net/11336/187838
identifier_str_mv Gutierrez, Silvina Gabriela; Petiti, Juan Pablo; Sosa, Liliana del Valle; Fozzatti, Laura; de Paul, Ana Lucia; et al.; 17β-oestradiol acts as a negative modulator of insulin-induced lactotroph cell proliferation through oestrogen receptor alpha, via nitric oxide/guanylyl cyclase/cGMP; Wiley Blackwell Publishing, Inc; Cell Proliferation; 43; 5; 10-2010; 505-514
0960-7722
1365-2184
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://onlinelibrary.wiley.com/doi/10.1111/j.1365-2184.2010.00700.x
info:eu-repo/semantics/altIdentifier/doi/10.1111/j.1365-2184.2010.00700.x
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 Wiley Blackwell Publishing, Inc
publisher.none.fl_str_mv Wiley Blackwell Publishing, Inc
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 12.982451

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