In: Progesterone2 Feb 2013
In the rodent uterus, epithelial cells proliferate in response to estrogen for the first few days of pregnancy. At Day 3 of pregnancy in the mouse and Day 4 of pregnancy in the rat, there is a proliferative switch from epithelial to stromal compartments. Stromal cells do not proliferate when progesterone receptor antagonists are used to block receptor function or when anti-progesterone antibodies are administered in early pregnancy. The number of synchronously dividing stromal cells in the rat endometrium increases in response to progesterone priming for 3 days followed by nidatory estrogen. Stromal cells are not responsive to estrogen in the absence of progesterone pretreatment, and the requirement for estrogen to initiate stromal cell proliferation can be bypassed when the endometrium of progesterone-primed animals is scratched by a needle or pinched with a hemostat. The endometrium of the ovariectomized rat can be sensitized to respond to a decidual stimulus when exposed to the appropriate sequence of sex steroids. In hormonally sensitized rats, progesterone alone increases DNA synthesis in uterine stromal cells, which later differentiate into deciduomal cells. The incorporation of labeled thymidine into polyploid decidual cells increases after progestin and estradiol treatment. However, once decidualization commences, progesterone alone stimulates DNA synthesis in polyploid deci-duomal cells. flovent inhaler
The case for progesterone control of stromal cell proliferation in the human endometrium is less well characterized. While epithelial and stromal cell proliferation is prevalent in the follicular phase of the menstrual cycle (estrogen dominance), there is a second wave of stromal cell proliferation in the last days of the luteal phase. Progesterone receptors are present in stromal cells at this time, suggesting that progesterone action controls this late wave of stromal cell mitosis.
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