Disrupted Cell Cycle Control in Cultured Endometrial Cells from Patients with Endometriosis Harboring the Progesterone Receptor Polymorphism PROGINS
Autor(a) principal: | |
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Data de Publicação: | 2009 |
Outros Autores: | , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNIFESP |
Texto Completo: | http://repositorio.unifesp.br/handle/11600/31626 http://dx.doi.org/10.2353/ajpath.2009.080966 |
Resumo: | Presently, little is understood about how endometriosis is established or maintained, or how genetic factors can predispose women to the disease. Because of the crucial role that the progesterone receptor polymorphism PROGINS plays in predisposing women to the development of endometriosis, we hypothesized that this variant may influence critical steps during endometrial cell metabolism that are involved in the pathogenesis of endometriosis. Eutopic endometria were collected from three sources: women with endometriosis who had a single PROGINS allele (from the progesterone receptor gene); women with endometriosis who had the wild-type progesterone receptor allele; and women without endometriosis who had the wild-type allele. Cells prepared from the eutopic endometria of these women were stimulated with both estradiol and progesterone, and then examined for cell proliferation, viability, and apoptosis. the cells from women with endometriosis that carried the PROGINS allele demonstrated increased proliferation, greater viability, and decreased apoptosis following progesterone treatment. in general, these parameters were very different as compared with those of women with endometriosis but without the PROGINS allele and women in the control group. This result indicates there is a reduced level of progesterone responsiveness in women who carry the PROGINS polymorphism. Because progesterone responsiveness is known to be an important characteristic of women with endometriosis, these data support the contention that the PROGINS polymorphism enhances the endometriosis phenotype. (Am J Pathol 2009, 175:215-224; DOI: 10.2353/ajpath.2009.080966) |
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D'Amora, Paulo [UNIFESP]Maciel, Thiago Trovati [UNIFESP]Tambellini, Rodrigo [UNIFESP]Mori, Marcelo A. [UNIFESP]Pesquero, João Bosco [UNIFESP]Sato, Helio [UNIFESP]Girão, Manoel João Batista Castello [UNIFESP]Silva, Ismael Dale Cotrim Guerreiro da [UNIFESP]Schor, Eduardo [UNIFESP]Universidade Federal de São Paulo (UNIFESP)2016-01-24T13:52:40Z2016-01-24T13:52:40Z2009-07-01American Journal of Pathology. Bethesda: Amer Soc Investigative Pathology, Inc, v. 175, n. 1, p. 215-224, 2009.0002-9440http://repositorio.unifesp.br/handle/11600/31626http://dx.doi.org/10.2353/ajpath.2009.08096610.2353/ajpath.2009.080966WOS:000267508600020Presently, little is understood about how endometriosis is established or maintained, or how genetic factors can predispose women to the disease. Because of the crucial role that the progesterone receptor polymorphism PROGINS plays in predisposing women to the development of endometriosis, we hypothesized that this variant may influence critical steps during endometrial cell metabolism that are involved in the pathogenesis of endometriosis. Eutopic endometria were collected from three sources: women with endometriosis who had a single PROGINS allele (from the progesterone receptor gene); women with endometriosis who had the wild-type progesterone receptor allele; and women without endometriosis who had the wild-type allele. Cells prepared from the eutopic endometria of these women were stimulated with both estradiol and progesterone, and then examined for cell proliferation, viability, and apoptosis. the cells from women with endometriosis that carried the PROGINS allele demonstrated increased proliferation, greater viability, and decreased apoptosis following progesterone treatment. in general, these parameters were very different as compared with those of women with endometriosis but without the PROGINS allele and women in the control group. This result indicates there is a reduced level of progesterone responsiveness in women who carry the PROGINS polymorphism. Because progesterone responsiveness is known to be an important characteristic of women with endometriosis, these data support the contention that the PROGINS polymorphism enhances the endometriosis phenotype. (Am J Pathol 2009, 175:215-224; DOI: 10.2353/ajpath.2009.080966)Universidade Federal de São Paulo, Dept Gynecol, Escola Paulista Med, Mol Gynecol & Proteom Lab,Plev Pain & Endometrios, BR-04039032 São Paulo, BrazilUniversidade Federal de São Paulo, Div Nephrol, Escola Paulista Med, BR-04039032 São Paulo, BrazilUniversidade Federal de São Paulo, Dept Biophys, Escola Paulista Med, BR-04039032 São Paulo, BrazilUniversidade Federal de São Paulo, Mol & Cell Biol Labs, Escola Paulista Med, BR-04039032 São Paulo, BrazilUniversidade Federal de São Paulo, Dept Gynecol, Escola Paulista Med, Mol Gynecol & Proteom Lab,Plev Pain & Endometrios, BR-04039032 São Paulo, BrazilUniversidade Federal de São Paulo, Div Nephrol, Escola Paulista Med, BR-04039032 São Paulo, BrazilUniversidade Federal de São Paulo, Dept Biophys, Escola Paulista Med, BR-04039032 São Paulo, BrazilUniversidade Federal de São Paulo, Mol & Cell Biol Labs, Escola Paulista Med, BR-04039032 São Paulo, BrazilWeb of Science215-224engAmer Soc Investigative Pathology, IncAmerican Journal of PathologyDisrupted Cell Cycle Control in Cultured Endometrial Cells from Patients with Endometriosis Harboring the Progesterone Receptor Polymorphism PROGINSinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP11600/316262022-07-08 10:28:58.829metadata only accessoai:repositorio.unifesp.br:11600/31626Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestopendoar:34652023-05-25T12:18:08.513428Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false |
dc.title.en.fl_str_mv |
Disrupted Cell Cycle Control in Cultured Endometrial Cells from Patients with Endometriosis Harboring the Progesterone Receptor Polymorphism PROGINS |
title |
Disrupted Cell Cycle Control in Cultured Endometrial Cells from Patients with Endometriosis Harboring the Progesterone Receptor Polymorphism PROGINS |
spellingShingle |
Disrupted Cell Cycle Control in Cultured Endometrial Cells from Patients with Endometriosis Harboring the Progesterone Receptor Polymorphism PROGINS D'Amora, Paulo [UNIFESP] |
title_short |
Disrupted Cell Cycle Control in Cultured Endometrial Cells from Patients with Endometriosis Harboring the Progesterone Receptor Polymorphism PROGINS |
title_full |
Disrupted Cell Cycle Control in Cultured Endometrial Cells from Patients with Endometriosis Harboring the Progesterone Receptor Polymorphism PROGINS |
title_fullStr |
Disrupted Cell Cycle Control in Cultured Endometrial Cells from Patients with Endometriosis Harboring the Progesterone Receptor Polymorphism PROGINS |
title_full_unstemmed |
Disrupted Cell Cycle Control in Cultured Endometrial Cells from Patients with Endometriosis Harboring the Progesterone Receptor Polymorphism PROGINS |
title_sort |
Disrupted Cell Cycle Control in Cultured Endometrial Cells from Patients with Endometriosis Harboring the Progesterone Receptor Polymorphism PROGINS |
author |
D'Amora, Paulo [UNIFESP] |
author_facet |
D'Amora, Paulo [UNIFESP] Maciel, Thiago Trovati [UNIFESP] Tambellini, Rodrigo [UNIFESP] Mori, Marcelo A. [UNIFESP] Pesquero, João Bosco [UNIFESP] Sato, Helio [UNIFESP] Girão, Manoel João Batista Castello [UNIFESP] Silva, Ismael Dale Cotrim Guerreiro da [UNIFESP] Schor, Eduardo [UNIFESP] |
author_role |
author |
author2 |
Maciel, Thiago Trovati [UNIFESP] Tambellini, Rodrigo [UNIFESP] Mori, Marcelo A. [UNIFESP] Pesquero, João Bosco [UNIFESP] Sato, Helio [UNIFESP] Girão, Manoel João Batista Castello [UNIFESP] Silva, Ismael Dale Cotrim Guerreiro da [UNIFESP] Schor, Eduardo [UNIFESP] |
author2_role |
author author author author author author author author |
dc.contributor.institution.none.fl_str_mv |
Universidade Federal de São Paulo (UNIFESP) |
dc.contributor.author.fl_str_mv |
D'Amora, Paulo [UNIFESP] Maciel, Thiago Trovati [UNIFESP] Tambellini, Rodrigo [UNIFESP] Mori, Marcelo A. [UNIFESP] Pesquero, João Bosco [UNIFESP] Sato, Helio [UNIFESP] Girão, Manoel João Batista Castello [UNIFESP] Silva, Ismael Dale Cotrim Guerreiro da [UNIFESP] Schor, Eduardo [UNIFESP] |
description |
Presently, little is understood about how endometriosis is established or maintained, or how genetic factors can predispose women to the disease. Because of the crucial role that the progesterone receptor polymorphism PROGINS plays in predisposing women to the development of endometriosis, we hypothesized that this variant may influence critical steps during endometrial cell metabolism that are involved in the pathogenesis of endometriosis. Eutopic endometria were collected from three sources: women with endometriosis who had a single PROGINS allele (from the progesterone receptor gene); women with endometriosis who had the wild-type progesterone receptor allele; and women without endometriosis who had the wild-type allele. Cells prepared from the eutopic endometria of these women were stimulated with both estradiol and progesterone, and then examined for cell proliferation, viability, and apoptosis. the cells from women with endometriosis that carried the PROGINS allele demonstrated increased proliferation, greater viability, and decreased apoptosis following progesterone treatment. in general, these parameters were very different as compared with those of women with endometriosis but without the PROGINS allele and women in the control group. This result indicates there is a reduced level of progesterone responsiveness in women who carry the PROGINS polymorphism. Because progesterone responsiveness is known to be an important characteristic of women with endometriosis, these data support the contention that the PROGINS polymorphism enhances the endometriosis phenotype. (Am J Pathol 2009, 175:215-224; DOI: 10.2353/ajpath.2009.080966) |
publishDate |
2009 |
dc.date.issued.fl_str_mv |
2009-07-01 |
dc.date.accessioned.fl_str_mv |
2016-01-24T13:52:40Z |
dc.date.available.fl_str_mv |
2016-01-24T13:52:40Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.citation.fl_str_mv |
American Journal of Pathology. Bethesda: Amer Soc Investigative Pathology, Inc, v. 175, n. 1, p. 215-224, 2009. |
dc.identifier.uri.fl_str_mv |
http://repositorio.unifesp.br/handle/11600/31626 http://dx.doi.org/10.2353/ajpath.2009.080966 |
dc.identifier.issn.none.fl_str_mv |
0002-9440 |
dc.identifier.doi.none.fl_str_mv |
10.2353/ajpath.2009.080966 |
dc.identifier.wos.none.fl_str_mv |
WOS:000267508600020 |
identifier_str_mv |
American Journal of Pathology. Bethesda: Amer Soc Investigative Pathology, Inc, v. 175, n. 1, p. 215-224, 2009. 0002-9440 10.2353/ajpath.2009.080966 WOS:000267508600020 |
url |
http://repositorio.unifesp.br/handle/11600/31626 http://dx.doi.org/10.2353/ajpath.2009.080966 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.ispartof.none.fl_str_mv |
American Journal of Pathology |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
215-224 |
dc.publisher.none.fl_str_mv |
Amer Soc Investigative Pathology, Inc |
publisher.none.fl_str_mv |
Amer Soc Investigative Pathology, Inc |
dc.source.none.fl_str_mv |
reponame:Repositório Institucional da UNIFESP instname:Universidade Federal de São Paulo (UNIFESP) instacron:UNIFESP |
instname_str |
Universidade Federal de São Paulo (UNIFESP) |
instacron_str |
UNIFESP |
institution |
UNIFESP |
reponame_str |
Repositório Institucional da UNIFESP |
collection |
Repositório Institucional da UNIFESP |
repository.name.fl_str_mv |
Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP) |
repository.mail.fl_str_mv |
|
_version_ |
1783460274120949760 |