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Original Studies |
Department of Obstetrics and Gynecology, Shiga University of Medical Science, Otsu 520-2192, Japan
Address all correspondence and requests for reprints to: Kenji Takakura, M.D., Department of Obstetrics and Gynecology, Shiga University of Medical Science, Seta Tsukinowa Cho, Otsu, 520-2192, Japan.
Although decidualization of endometrial stromal cells (ESC) is crucial for blastocyst implantation and maintenance of pregnancy, its complex mechanism still remains largely unknown. It has long been believed that hCG can directly induce in vitro decidualization of ESC via cAMP signaling. Recently, however, it has been reported that the LH/CG receptor is not present in human endometrium, and the direct effect of hCG on decidualization has become controversial. To reevaluate the exact effect of hCG on decidualization, human ESC were isolated and cultured with hCG and/or ovarian steroids.
ESC treated with 17ß-estradiol plus progesterone (E2/P) transformed morphologically and produced significant PRL, whereas ESC treated with hCG alone showed no significant increase in PRL in culture medium and exhibited no morphological changes. Moreover, hCG did not promote E2/P-induced PRL production or intracellular cAMP accumulation, and protein kinase A inhibitor failed to block E2/P-induced PRL production.
These results suggest that hCG does not directly affect in vitro decidualization of human ESC and that the process of E2/P-induced in vitro decidualization might consist of several pathways, including the intracellular cAMP signaling cascade.
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