Progestin activation of nongenomic pathways via cross talk of progesterone receptor with estrogen receptor β induces proliferation of endometrial stromal cells
Uterine decidualization is characterized by stromal cell proliferation and differentiation, which are controlled by ovarian hormones estradiol and progesterone. Here we report that the proliferative response of UIII rat uterine stromal cells to a short treatment with progestins requires active proge...
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2005
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Acceso en línea: | http://hdl.handle.net/20.500.12110/paper_08888809_v19_n12_p3023_Vallejo |
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paperaa:paper_08888809_v19_n12_p3023_Vallejo2023-06-12T16:48:21Z Progestin activation of nongenomic pathways via cross talk of progesterone receptor with estrogen receptor β induces proliferation of endometrial stromal cells Mol. Endocrinol. 2005;19(12):3023-3037 Vallejo, G. Ballaré, C. Barañao, J.L. Beato, M. Saragüeta, P. estradiol estrogen receptor beta fulvestrant gestagen mifepristone mitogen activated protein kinase 1 mitogen activated protein kinase 3 progesterone receptor promegestone animal cell article cell differentiation cell nucleus membrane cell proliferation controlled study decidualization endometrium cell enzyme activation estrogen activity female hormonal regulation immunoprecipitation nonhuman priority journal progesterone release protein cross linking protein localization rat reporter gene signal transduction stroma cell uterine cervix ripening Active Transport, Cell Nucleus Animals Cell Nucleus Cell Proliferation Cytoplasm Endometrium Enzyme Activation Estrogen Receptor alpha Estrogen Receptor beta Female Genes, Reporter Genome Mitogen-Activated Protein Kinase 1 Mitogen-Activated Protein Kinase 3 Mutation Progestins Promegestone Proto-Oncogene Proteins c-akt Rats Receptors, Progesterone Signal Transduction Stromal Cells Trans-Activation (Genetics) Transcription, Genetic Animalia Uterine decidualization is characterized by stromal cell proliferation and differentiation, which are controlled by ovarian hormones estradiol and progesterone. Here we report that the proliferative response of UIII rat uterine stromal cells to a short treatment with progestins requires active progesterone receptor (PR) and estrogen receptor β (ERβ) as well as a rapid and transient activation of Erk1-2 and Akt signaling. The optimal R5020 concentration for the proliferative response as well as for activation of the signaling cascades was between 10 and 100 pM. UIII cells are negative for ERα and have low levels of ERβ and PR located mainly in the cytoplasm. Upon progestin treatment PR translocated to the cell nucleus where it colocalized with activated Erk1-2. Neither progestins nor estradiol transactivated the corresponding transfected reporter genes, suggesting that endogenous PR and ERβ are transcriptionally incompetent. A fraction of endogenous PR and ERβ form a complex as demonstrated by coimmunoprecipitation. Taken together, our results suggest that the proliferative response of uterine stromal cells to picomolar concentrations of progestins does not require direct transcriptional effects and is mediated by activation of the Erk1-2 and Akt signaling pathways via cross talk between PR and ERβ. Copyright © 2005 by The Endocrine Society. Fil:Vallejo, G. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Ballaré, C. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Barañao, J.L. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Saragüeta, P. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. 2005 info:eu-repo/semantics/article info:ar-repo/semantics/artículo info:eu-repo/semantics/publishedVersion application/pdf eng info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar http://hdl.handle.net/20.500.12110/paper_08888809_v19_n12_p3023_Vallejo |
institution |
Universidad de Buenos Aires |
institution_str |
I-28 |
repository_str |
R-134 |
collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
language |
Inglés |
orig_language_str_mv |
eng |
topic |
estradiol estrogen receptor beta fulvestrant gestagen mifepristone mitogen activated protein kinase 1 mitogen activated protein kinase 3 progesterone receptor promegestone animal cell article cell differentiation cell nucleus membrane cell proliferation controlled study decidualization endometrium cell enzyme activation estrogen activity female hormonal regulation immunoprecipitation nonhuman priority journal progesterone release protein cross linking protein localization rat reporter gene signal transduction stroma cell uterine cervix ripening Active Transport, Cell Nucleus Animals Cell Nucleus Cell Proliferation Cytoplasm Endometrium Enzyme Activation Estrogen Receptor alpha Estrogen Receptor beta Female Genes, Reporter Genome Mitogen-Activated Protein Kinase 1 Mitogen-Activated Protein Kinase 3 Mutation Progestins Promegestone Proto-Oncogene Proteins c-akt Rats Receptors, Progesterone Signal Transduction Stromal Cells Trans-Activation (Genetics) Transcription, Genetic Animalia |
spellingShingle |
estradiol estrogen receptor beta fulvestrant gestagen mifepristone mitogen activated protein kinase 1 mitogen activated protein kinase 3 progesterone receptor promegestone animal cell article cell differentiation cell nucleus membrane cell proliferation controlled study decidualization endometrium cell enzyme activation estrogen activity female hormonal regulation immunoprecipitation nonhuman priority journal progesterone release protein cross linking protein localization rat reporter gene signal transduction stroma cell uterine cervix ripening Active Transport, Cell Nucleus Animals Cell Nucleus Cell Proliferation Cytoplasm Endometrium Enzyme Activation Estrogen Receptor alpha Estrogen Receptor beta Female Genes, Reporter Genome Mitogen-Activated Protein Kinase 1 Mitogen-Activated Protein Kinase 3 Mutation Progestins Promegestone Proto-Oncogene Proteins c-akt Rats Receptors, Progesterone Signal Transduction Stromal Cells Trans-Activation (Genetics) Transcription, Genetic Animalia Vallejo, G. Ballaré, C. Barañao, J.L. Beato, M. Saragüeta, P. Progestin activation of nongenomic pathways via cross talk of progesterone receptor with estrogen receptor β induces proliferation of endometrial stromal cells |
topic_facet |
estradiol estrogen receptor beta fulvestrant gestagen mifepristone mitogen activated protein kinase 1 mitogen activated protein kinase 3 progesterone receptor promegestone animal cell article cell differentiation cell nucleus membrane cell proliferation controlled study decidualization endometrium cell enzyme activation estrogen activity female hormonal regulation immunoprecipitation nonhuman priority journal progesterone release protein cross linking protein localization rat reporter gene signal transduction stroma cell uterine cervix ripening Active Transport, Cell Nucleus Animals Cell Nucleus Cell Proliferation Cytoplasm Endometrium Enzyme Activation Estrogen Receptor alpha Estrogen Receptor beta Female Genes, Reporter Genome Mitogen-Activated Protein Kinase 1 Mitogen-Activated Protein Kinase 3 Mutation Progestins Promegestone Proto-Oncogene Proteins c-akt Rats Receptors, Progesterone Signal Transduction Stromal Cells Trans-Activation (Genetics) Transcription, Genetic Animalia |
description |
Uterine decidualization is characterized by stromal cell proliferation and differentiation, which are controlled by ovarian hormones estradiol and progesterone. Here we report that the proliferative response of UIII rat uterine stromal cells to a short treatment with progestins requires active progesterone receptor (PR) and estrogen receptor β (ERβ) as well as a rapid and transient activation of Erk1-2 and Akt signaling. The optimal R5020 concentration for the proliferative response as well as for activation of the signaling cascades was between 10 and 100 pM. UIII cells are negative for ERα and have low levels of ERβ and PR located mainly in the cytoplasm. Upon progestin treatment PR translocated to the cell nucleus where it colocalized with activated Erk1-2. Neither progestins nor estradiol transactivated the corresponding transfected reporter genes, suggesting that endogenous PR and ERβ are transcriptionally incompetent. A fraction of endogenous PR and ERβ form a complex as demonstrated by coimmunoprecipitation. Taken together, our results suggest that the proliferative response of uterine stromal cells to picomolar concentrations of progestins does not require direct transcriptional effects and is mediated by activation of the Erk1-2 and Akt signaling pathways via cross talk between PR and ERβ. Copyright © 2005 by The Endocrine Society. |
format |
Artículo Artículo publishedVersion |
author |
Vallejo, G. Ballaré, C. Barañao, J.L. Beato, M. Saragüeta, P. |
author_facet |
Vallejo, G. Ballaré, C. Barañao, J.L. Beato, M. Saragüeta, P. |
author_sort |
Vallejo, G. |
title |
Progestin activation of nongenomic pathways via cross talk of progesterone receptor with estrogen receptor β induces proliferation of endometrial stromal cells |
title_short |
Progestin activation of nongenomic pathways via cross talk of progesterone receptor with estrogen receptor β induces proliferation of endometrial stromal cells |
title_full |
Progestin activation of nongenomic pathways via cross talk of progesterone receptor with estrogen receptor β induces proliferation of endometrial stromal cells |
title_fullStr |
Progestin activation of nongenomic pathways via cross talk of progesterone receptor with estrogen receptor β induces proliferation of endometrial stromal cells |
title_full_unstemmed |
Progestin activation of nongenomic pathways via cross talk of progesterone receptor with estrogen receptor β induces proliferation of endometrial stromal cells |
title_sort |
progestin activation of nongenomic pathways via cross talk of progesterone receptor with estrogen receptor β induces proliferation of endometrial stromal cells |
publishDate |
2005 |
url |
http://hdl.handle.net/20.500.12110/paper_08888809_v19_n12_p3023_Vallejo |
work_keys_str_mv |
AT vallejog progestinactivationofnongenomicpathwaysviacrosstalkofprogesteronereceptorwithestrogenreceptorbinducesproliferationofendometrialstromalcells AT ballarec progestinactivationofnongenomicpathwaysviacrosstalkofprogesteronereceptorwithestrogenreceptorbinducesproliferationofendometrialstromalcells AT baranaojl progestinactivationofnongenomicpathwaysviacrosstalkofprogesteronereceptorwithestrogenreceptorbinducesproliferationofendometrialstromalcells AT beatom progestinactivationofnongenomicpathwaysviacrosstalkofprogesteronereceptorwithestrogenreceptorbinducesproliferationofendometrialstromalcells AT saraguetap progestinactivationofnongenomicpathwaysviacrosstalkofprogesteronereceptorwithestrogenreceptorbinducesproliferationofendometrialstromalcells |
_version_ |
1769810339568812032 |