Developmental programming: prenatal steroid excess disrupts key members of intra-ovarian steroidogenic pathway in sheep

Autores
Padmanabhan, Vasantha; Salvetti, Natalia Raquel; Matiller, Valentina; Ortega, Hugo Hector
Año de publicación
2014
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Prenatal testosterone (T) excess disrupts ovarian cyclicity and increases circulating estradiol levels as well as follicular recruitment and persistence culminating in multifollicular ovary similar to women with polycystic ovary syndrome. We tested whether prenatal T excess, by androgenic or estrogenic action, disrupts the steroid biosynthetic machinery in sheep in a cell-, follicle stage-, age-, and treatment-specific manner consistent with the ovarian disruptions and increased estradiol release. Impact of T/dihydrotestosterone (DHT) treatments from days 30?90 of gestation on steroidogenic acute regulatory protein, 3-hydroxysteroid dehydrogenase, cytochrome P-450 17-hydroxylase/C17, 20-lyase (CYP17A1), and CYP19A1 were examined on fetal day 90, 140 and 10 months (postpubertal), and 21 months (adult, no DHT group) of age by immunohistochemistry. All
4 markers changed in a cell-, follicle stage-, and age-specific manner. Both treatments increased steroidogenic acute regulatory protein expression in preantral follicles of postpubertal and adult females. Effects of prenatal T and DHT on 3-hydroxysteroid dehydrogenase differed in a follicleand age-specific manner. CYP17A1 was reduced in the theca interna of antral follicles by T, but not DHT, in 10- and 21-month-old females. CYP19A1 was reduced by both T and DHT at all ages barring an increase on fetal day 140. Reduced granulosa CYP19A1 and thecal CYP17A1 in adults likely disrupt the intrafollicular androgen/estrogen balance contributing to follicular persistence. The
reduced thecal CYP17A1 expression suggests that the hyperandrogenic ovarian phenotype may originate from increased enzyme activity or alternatively via a different isoform of CYP17. The reduced CYP19A1 in antral follicles of adults indicates that the increased circulating estradiol release likely arises from the increased number of persisting follicles.
Fil: Padmanabhan, Vasantha. Michigan State University; Estados Unidos
Fil: Salvetti, Natalia Raquel. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Santa Fe. Instituto de Ciencias Veterinarias del Litoral. Universidad Nacional del Litoral. Facultad de Cs.veterinarias. Instituto de Ciencias Veterinarias del Litoral; Argentina
Fil: Matiller, Valentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Santa Fe. Instituto de Ciencias Veterinarias del Litoral. Universidad Nacional del Litoral. Facultad de Cs.veterinarias. Instituto de Ciencias Veterinarias del Litoral; Argentina
Fil: Ortega, Hugo Hector. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Santa Fe. Instituto de Ciencias Veterinarias del Litoral. Universidad Nacional del Litoral. Facultad de Cs.veterinarias. Instituto de Ciencias Veterinarias del Litoral; Argentina
Materia
Androgens
Immunohistochemistry
Estradiol
Adult
Aromatase
Fetus
Hair Follicle
Ovarian Follicle
Sheep
Steroid 17-Alpha-Monooxygenase
Steroids
Ovary
Prenatal Care
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:11336/20962

id CONICETDig_48f4f00dc0aada2ee449501d442cdfbc
oai_identifier_str oai:ri.conicet.gov.ar:11336/20962
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Developmental programming: prenatal steroid excess disrupts key members of intra-ovarian steroidogenic pathway in sheepPadmanabhan, VasanthaSalvetti, Natalia RaquelMatiller, ValentinaOrtega, Hugo HectorAndrogensImmunohistochemistryEstradiolAdultAromataseFetusHair FollicleOvarian FollicleSheepSteroid 17-Alpha-MonooxygenaseSteroidsOvaryPrenatal Carehttps://purl.org/becyt/ford/4.3https://purl.org/becyt/ford/4Prenatal testosterone (T) excess disrupts ovarian cyclicity and increases circulating estradiol levels as well as follicular recruitment and persistence culminating in multifollicular ovary similar to women with polycystic ovary syndrome. We tested whether prenatal T excess, by androgenic or estrogenic action, disrupts the steroid biosynthetic machinery in sheep in a cell-, follicle stage-, age-, and treatment-specific manner consistent with the ovarian disruptions and increased estradiol release. Impact of T/dihydrotestosterone (DHT) treatments from days 30?90 of gestation on steroidogenic acute regulatory protein, 3-hydroxysteroid dehydrogenase, cytochrome P-450 17-hydroxylase/C17, 20-lyase (CYP17A1), and CYP19A1 were examined on fetal day 90, 140 and 10 months (postpubertal), and 21 months (adult, no DHT group) of age by immunohistochemistry. All<br />4 markers changed in a cell-, follicle stage-, and age-specific manner. Both treatments increased steroidogenic acute regulatory protein expression in preantral follicles of postpubertal and adult females. Effects of prenatal T and DHT on 3-hydroxysteroid dehydrogenase differed in a follicleand age-specific manner. CYP17A1 was reduced in the theca interna of antral follicles by T, but not DHT, in 10- and 21-month-old females. CYP19A1 was reduced by both T and DHT at all ages barring an increase on fetal day 140. Reduced granulosa CYP19A1 and thecal CYP17A1 in adults likely disrupt the intrafollicular androgen/estrogen balance contributing to follicular persistence. The<br />reduced thecal CYP17A1 expression suggests that the hyperandrogenic ovarian phenotype may originate from increased enzyme activity or alternatively via a different isoform of CYP17. The reduced CYP19A1 in antral follicles of adults indicates that the increased circulating estradiol release likely arises from the increased number of persisting follicles.Fil: Padmanabhan, Vasantha. Michigan State University; Estados UnidosFil: Salvetti, Natalia Raquel. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Santa Fe. Instituto de Ciencias Veterinarias del Litoral. Universidad Nacional del Litoral. Facultad de Cs.veterinarias. Instituto de Ciencias Veterinarias del Litoral; ArgentinaFil: Matiller, Valentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Santa Fe. Instituto de Ciencias Veterinarias del Litoral. Universidad Nacional del Litoral. Facultad de Cs.veterinarias. Instituto de Ciencias Veterinarias del Litoral; ArgentinaFil: Ortega, Hugo Hector. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Santa Fe. Instituto de Ciencias Veterinarias del Litoral. Universidad Nacional del Litoral. Facultad de Cs.veterinarias. Instituto de Ciencias Veterinarias del Litoral; ArgentinaOxford University Press2014-08info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/20962Padmanabhan, Vasantha; Salvetti, Natalia Raquel; Matiller, Valentina; Ortega, Hugo Hector; Developmental programming: prenatal steroid excess disrupts key members of intra-ovarian steroidogenic pathway in sheep; Oxford University Press; Endocrinology; 155; 9; 8-2014; 3649-36600013-72271945-7170CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1210/en.2014-1266info:eu-repo/semantics/altIdentifier/url/https://academic.oup.com/endo/article-lookup/doi/10.1210/en.2014-1266info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:47:32Zoai:ri.conicet.gov.ar:11336/20962instacron: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 09:47:32.79CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Developmental programming: prenatal steroid excess disrupts key members of intra-ovarian steroidogenic pathway in sheep
title Developmental programming: prenatal steroid excess disrupts key members of intra-ovarian steroidogenic pathway in sheep
spellingShingle Developmental programming: prenatal steroid excess disrupts key members of intra-ovarian steroidogenic pathway in sheep
Padmanabhan, Vasantha
Androgens
Immunohistochemistry
Estradiol
Adult
Aromatase
Fetus
Hair Follicle
Ovarian Follicle
Sheep
Steroid 17-Alpha-Monooxygenase
Steroids
Ovary
Prenatal Care
title_short Developmental programming: prenatal steroid excess disrupts key members of intra-ovarian steroidogenic pathway in sheep
title_full Developmental programming: prenatal steroid excess disrupts key members of intra-ovarian steroidogenic pathway in sheep
title_fullStr Developmental programming: prenatal steroid excess disrupts key members of intra-ovarian steroidogenic pathway in sheep
title_full_unstemmed Developmental programming: prenatal steroid excess disrupts key members of intra-ovarian steroidogenic pathway in sheep
title_sort Developmental programming: prenatal steroid excess disrupts key members of intra-ovarian steroidogenic pathway in sheep
dc.creator.none.fl_str_mv Padmanabhan, Vasantha
Salvetti, Natalia Raquel
Matiller, Valentina
Ortega, Hugo Hector
author Padmanabhan, Vasantha
author_facet Padmanabhan, Vasantha
Salvetti, Natalia Raquel
Matiller, Valentina
Ortega, Hugo Hector
author_role author
author2 Salvetti, Natalia Raquel
Matiller, Valentina
Ortega, Hugo Hector
author2_role author
author
author
dc.subject.none.fl_str_mv Androgens
Immunohistochemistry
Estradiol
Adult
Aromatase
Fetus
Hair Follicle
Ovarian Follicle
Sheep
Steroid 17-Alpha-Monooxygenase
Steroids
Ovary
Prenatal Care
topic Androgens
Immunohistochemistry
Estradiol
Adult
Aromatase
Fetus
Hair Follicle
Ovarian Follicle
Sheep
Steroid 17-Alpha-Monooxygenase
Steroids
Ovary
Prenatal Care
purl_subject.fl_str_mv https://purl.org/becyt/ford/4.3
https://purl.org/becyt/ford/4
dc.description.none.fl_txt_mv Prenatal testosterone (T) excess disrupts ovarian cyclicity and increases circulating estradiol levels as well as follicular recruitment and persistence culminating in multifollicular ovary similar to women with polycystic ovary syndrome. We tested whether prenatal T excess, by androgenic or estrogenic action, disrupts the steroid biosynthetic machinery in sheep in a cell-, follicle stage-, age-, and treatment-specific manner consistent with the ovarian disruptions and increased estradiol release. Impact of T/dihydrotestosterone (DHT) treatments from days 30?90 of gestation on steroidogenic acute regulatory protein, 3-hydroxysteroid dehydrogenase, cytochrome P-450 17-hydroxylase/C17, 20-lyase (CYP17A1), and CYP19A1 were examined on fetal day 90, 140 and 10 months (postpubertal), and 21 months (adult, no DHT group) of age by immunohistochemistry. All<br />4 markers changed in a cell-, follicle stage-, and age-specific manner. Both treatments increased steroidogenic acute regulatory protein expression in preantral follicles of postpubertal and adult females. Effects of prenatal T and DHT on 3-hydroxysteroid dehydrogenase differed in a follicleand age-specific manner. CYP17A1 was reduced in the theca interna of antral follicles by T, but not DHT, in 10- and 21-month-old females. CYP19A1 was reduced by both T and DHT at all ages barring an increase on fetal day 140. Reduced granulosa CYP19A1 and thecal CYP17A1 in adults likely disrupt the intrafollicular androgen/estrogen balance contributing to follicular persistence. The<br />reduced thecal CYP17A1 expression suggests that the hyperandrogenic ovarian phenotype may originate from increased enzyme activity or alternatively via a different isoform of CYP17. The reduced CYP19A1 in antral follicles of adults indicates that the increased circulating estradiol release likely arises from the increased number of persisting follicles.
Fil: Padmanabhan, Vasantha. Michigan State University; Estados Unidos
Fil: Salvetti, Natalia Raquel. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Santa Fe. Instituto de Ciencias Veterinarias del Litoral. Universidad Nacional del Litoral. Facultad de Cs.veterinarias. Instituto de Ciencias Veterinarias del Litoral; Argentina
Fil: Matiller, Valentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Santa Fe. Instituto de Ciencias Veterinarias del Litoral. Universidad Nacional del Litoral. Facultad de Cs.veterinarias. Instituto de Ciencias Veterinarias del Litoral; Argentina
Fil: Ortega, Hugo Hector. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Santa Fe. Instituto de Ciencias Veterinarias del Litoral. Universidad Nacional del Litoral. Facultad de Cs.veterinarias. Instituto de Ciencias Veterinarias del Litoral; Argentina
description Prenatal testosterone (T) excess disrupts ovarian cyclicity and increases circulating estradiol levels as well as follicular recruitment and persistence culminating in multifollicular ovary similar to women with polycystic ovary syndrome. We tested whether prenatal T excess, by androgenic or estrogenic action, disrupts the steroid biosynthetic machinery in sheep in a cell-, follicle stage-, age-, and treatment-specific manner consistent with the ovarian disruptions and increased estradiol release. Impact of T/dihydrotestosterone (DHT) treatments from days 30?90 of gestation on steroidogenic acute regulatory protein, 3-hydroxysteroid dehydrogenase, cytochrome P-450 17-hydroxylase/C17, 20-lyase (CYP17A1), and CYP19A1 were examined on fetal day 90, 140 and 10 months (postpubertal), and 21 months (adult, no DHT group) of age by immunohistochemistry. All<br />4 markers changed in a cell-, follicle stage-, and age-specific manner. Both treatments increased steroidogenic acute regulatory protein expression in preantral follicles of postpubertal and adult females. Effects of prenatal T and DHT on 3-hydroxysteroid dehydrogenase differed in a follicleand age-specific manner. CYP17A1 was reduced in the theca interna of antral follicles by T, but not DHT, in 10- and 21-month-old females. CYP19A1 was reduced by both T and DHT at all ages barring an increase on fetal day 140. Reduced granulosa CYP19A1 and thecal CYP17A1 in adults likely disrupt the intrafollicular androgen/estrogen balance contributing to follicular persistence. The<br />reduced thecal CYP17A1 expression suggests that the hyperandrogenic ovarian phenotype may originate from increased enzyme activity or alternatively via a different isoform of CYP17. The reduced CYP19A1 in antral follicles of adults indicates that the increased circulating estradiol release likely arises from the increased number of persisting follicles.
publishDate 2014
dc.date.none.fl_str_mv 2014-08
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/11336/20962
Padmanabhan, Vasantha; Salvetti, Natalia Raquel; Matiller, Valentina; Ortega, Hugo Hector; Developmental programming: prenatal steroid excess disrupts key members of intra-ovarian steroidogenic pathway in sheep; Oxford University Press; Endocrinology; 155; 9; 8-2014; 3649-3660
0013-7227
1945-7170
CONICET Digital
CONICET
url http://hdl.handle.net/11336/20962
identifier_str_mv Padmanabhan, Vasantha; Salvetti, Natalia Raquel; Matiller, Valentina; Ortega, Hugo Hector; Developmental programming: prenatal steroid excess disrupts key members of intra-ovarian steroidogenic pathway in sheep; Oxford University Press; Endocrinology; 155; 9; 8-2014; 3649-3660
0013-7227
1945-7170
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1210/en.2014-1266
info:eu-repo/semantics/altIdentifier/url/https://academic.oup.com/endo/article-lookup/doi/10.1210/en.2014-1266
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
application/pdf
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)
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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