Abstract
Objective: During the secretory phase of the menstrual cycle, progesterone induces the activity of 17-βHSD type 2 which metabolizes estradiol to an inactive steroid estrone in endometrial epithelial cells. Our prior studies indicated that progesterone-dependent paracrine factors from stromal cells upregulate the expression of 17-βHSD type 2 in human endometrial epithelial cells. We also found that the transcription factor Sp1 in epithelial cells mediated the induction of 17-βHSD type 2 by paracrine factors secreted from stromal cells. In other systems, the stimulatory transcription factor Sp3 acts as surrogate Sp1, whereas the inhibitory transcription factor early growth response-1 (Egr-1) differentially regulated the expression of many genes via common Sp1/Sp3/Egr-1 binding sites in their promoter regions. Sp1, Sp3 and Egr-1 were demonstrated in the human endometrium. Thus, we sought to determine herein the possible role of Egr-1 in modulating the induction by Sp1 or Sp3 of the 17-βHSD type 2 gene in human endometrial epithelial cells.
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