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Abstract:

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.

Registro:

Documento: Artículo
Título:Progestin activation of nongenomic pathways via cross talk of progesterone receptor with estrogen receptor β induces proliferation of endometrial stromal cells
Autor:Vallejo, G.; Ballaré, C.; Barañao, J.L.; Beato, M.; Saragüeta, P.
Filiación:Instituto de Biología Y Medicina Experimental, Consejo Nacional de Investigaciones Científicas Y Técnicas, Universidad de Buenos Aires, 1428 Buenos Aires, Argentina
Departamento de Química Biológica, Facultad de Ciencias Exactas Y Naturales, Universidad de Buenos Aires, 1428 Buenos Aires, Argentina
Centre de Regulació Genòmica, Universitat Pompeu Fabra, 08003 Barcelona, Spain
Instituto de Biología Y Medicina Experimental (IBYME-CONICET), Obligado 2490, (1428) Buenos Aires, Argentina
Palabras clave: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
Año:2005
Volumen:19
Número:12
Página de inicio:3023
Página de fin:3037
DOI: http://dx.doi.org/10.1210/me.2005-0016
Handle:http://hdl.handle.net/20.500.12110/paper_08888809_v19_n12_p3023_Vallejo
Título revista:Molecular Endocrinology
Título revista abreviado:Mol. Endocrinol.
ISSN:08888809
CODEN:MOENE
CAS:estradiol, 50-28-2; fulvestrant, 129453-61-8; mifepristone, 84371-65-3; mitogen activated protein kinase 1, 137632-08-7; mitogen activated protein kinase 3, 137632-07-6; promegestone, 34184-77-5; Estrogen Receptor alpha; Estrogen Receptor beta; Mitogen-Activated Protein Kinase 1, EC 2.7.1.37; Mitogen-Activated Protein Kinase 3, EC 2.7.1.37; Progestins; Promegestone, 34184-77-5; Proto-Oncogene Proteins c-akt, EC 2.7.1.37; Receptors, Progesterone
PDF:https://bibliotecadigital.exactas.uba.ar/download/paper/paper_08888809_v19_n12_p3023_Vallejo.pdf
Registro:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_08888809_v19_n12_p3023_Vallejo

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Citas:

---------- APA ----------
Vallejo, G., Ballaré, C., Barañao, J.L., Beato, M. & Saragüeta, P. (2005) . Progestin activation of nongenomic pathways via cross talk of progesterone receptor with estrogen receptor β induces proliferation of endometrial stromal cells. Molecular Endocrinology, 19(12), 3023-3037.
http://dx.doi.org/10.1210/me.2005-0016
---------- CHICAGO ----------
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" . Molecular Endocrinology 19, no. 12 (2005) : 3023-3037.
http://dx.doi.org/10.1210/me.2005-0016
---------- MLA ----------
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" . Molecular Endocrinology, vol. 19, no. 12, 2005, pp. 3023-3037.
http://dx.doi.org/10.1210/me.2005-0016
---------- VANCOUVER ----------
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. Mol. Endocrinol. 2005;19(12):3023-3037.
http://dx.doi.org/10.1210/me.2005-0016