Progesterone-Growth Factor Interactions in Uterine Stromal Cells: STEROIDS CONTROL ENDOMETRIAL CELL PROLIFERATION(2)

In: Progesterone

3 Feb 2013

ENDOMETRIAL CELL PROLIFERATION(2)

During the luteal phase of the menstrual cycle, extensive vascular development and differentiation of stromal cells into decidual cells occur in response to ovarian hormones, in particular progesterone. These biochemical changes in the uterine stroma of women resemble those that take place during the implantation reaction in rodents. However, these cellular alterations occur spontaneously in women, while in rodents, a blastocyst or external stimulus is required. Whether this difference is due to the aggressive nature of the human trophoblast, as suggested by Finn, remains to be demonstrated. birth control pills

Only a few maternally expressed factors such as colony stimulating factor-1, leukemia inhibitory factor, and progesterone, are absolutely necessary for implantation. While interactions between progesterone and estrogen in many species normally affect target tissues, only progesterone is required for the establishment of pregnancy in all mammals studied to date. Even in species such as the mouse, where estrogen action is normally compulsory, epidermal growth factor can substitute for estrogen in promoting blastocyst implantation during embryonic delay. Since progesterone is the hormone of pregnancy, it is imperative that its molecular mechanisms of action on uterine cell proliferation and differentiation be elucidated. Progress in this area is expected since mice lacking the progesterone receptor exhibit defects in all reproductive tissues. The uterine stromal cells in the progesterone receptor ‘‘knockout’’ mouse are unable to undergo a decidual cell reaction, and the uterus exhibits hyperplasia and inflammation. Since progesterone is a pleiotropic regulator of multiple aspects of reproduction in vivo, development of an in vitro system that can specifically address progesterone control of cell proliferation is an essential complement to the progesterone receptor knockout model.


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