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Submitted on January 10, 2005
Accepted on June 28, 2005
induces proliferation of endometrial stromal cells
Instituto de Biología y Medicina Experimental, IByME-CONICET and Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales Universidad de Buenos Aires, Obligado 2490, (1428) Buenos Aires Argentina; Centre de Regulació Genòmica (CRG), UPF, Passeig Marítim 37-49, (08003) Barcelona, Spain
* To whom correspondence should be addressed. E-mail: sarag{at}dna.uba.ar.
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 beta (ER
) 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 y 100 pM. UIII cells are negative for ER
and have low levels of ER 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 ER are transcriptionally incompetent. A fraction of endogenous PR and ER form a complex as demonstrated by co-immunoprecipitation. 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 crosstalk between PR and ER.
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