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Expression of the molecules that modulate the synthesis and action of estrogen in, or reflect function of, Sertoli cells was determined in the fetal testis of baboons in which estrogen levels were suppressed in the second half of gestation to determine whether this may account for the previously reported alteration in fetal testis germ cell development. P-450 aromatase, estrogen receptor (ER) β, and α-inhibin protein assessed by immunocytochemistry was abundantly expressed in Sertoli cells of the fetal baboon testis, but unaltered in baboons in which estrogen levels were suppressed by letrozole administration. Moreover, P-450 aromatase and ERα and β mRNA levels, assessed by real-time RT-PCR, were similar in germ/Sertoli cells and interstitial cells isolated from the fetal testis of untreated and letrozole-treated baboons. These results indicate that expression of the proteins that modulate the formation and action of estrogen in, and function of, Sertoli cells is not responsible for the changes in germ cell development in the fetal testis of estrogen-deprived baboons.

Vascular smooth muscle cell (VSMC) migration is a pivotal early step in blood vessel remodeling; however, very little is known about the regulation of this process in the human endometrium during the menstrual cycle. In this study, explants of human endometrium were incubated with estradiol and/or progesterone and the conditioned medium (CM) applied to cultures of VSMC to test the hypothesis that estrogen and progesterone stimulate endometrial cells to secrete a factor(s) that promotes VSMC migration. Endometrial explants were composed of highly organized glands and stroma. VSMC migration (cells migrated in 21 h/mm2 fibronectin-coated semipermeable membrane) in the presence of CM from human endometrial explants obtained in the proliferative phase of the menstrual cycle and incubated for 24 h with estradiol was approximately threefold greater (P < 0.001) than with medium alone and greater (P < 0.05) than with CM from explants treated with estradiol plus progesterone or progesterone. It is concluded, therefore, that estrogen stimulates endometrial secretion of a factor(s) that promotes VSMC migration as an early step in vessel remodeling within the endometrium.