Abstract
Background: Wilm’s tumor 1 gene (WT1) is a transcription factor with versatile cellular functions in embryonic development, the maintenance of adult tissue functions, and regeneration. WT1 is known to be regulated by progesterone and it is abundantly expressed in endometrium, but its function is unclear. Design: in this observational and descriptive study, WT1 expression was detected by immunohistochemical staining in endometrium of various physiological and pathological conditions. Result: WT1 was detected in endometrial stromal cells and vascular smooth muscle cells, in both proliferative and secretory phases of menstrual cycles. WT1 appeared increased in vascular smooth muscle cells in spiral artery in early pregnancy and it was also detected in regenerative endothelial cells and smooth muscle cells in decidual vasculopathy at term. WT1 expression appeared decreased in endometrial stromal cells in adenomyosis (endometriosis). Conclusion: WT1 potentially links the hormonal effects on endometrial decidualization and may play a role in gestational vascular transformation during pregnancy and restoration after pregnancy.
Highlights
Endometrial decidualization is characterized by the morphological transformation of epithelium, endometrial stromal tissue and terminal segments of the spiral artery, through the concerted action of steroid hormones, secreted by the ovary and subsequently corpus luteum after ovulation [1,2]
The Wilm’s tumor 1 gene (WT1) function in endometrium appeared at least in part to be through regulation by the steroid hormones and insulin-like growth factors (IGF), which are known to be critical for decidualization, implantation and fetal development [25,26,27]
Our current WT1 expression data in endometrium is consistent with the known function of progesterone in both menstrual cycles and pregnancy
Summary
Endometrial decidualization is characterized by the morphological transformation of epithelium, endometrial stromal tissue and terminal segments of the spiral artery, through the concerted action of steroid hormones (estrogen and progesterone), secreted by the ovary and subsequently corpus luteum after ovulation [1,2]. Extravillous trophoblasts derived from the early trophectoderm invade the decidualized endometrial stromal tissue and the spiral artery, leading to trophoblasts-dependent spiral artery remodeling, by forming the endovascular trophoblastic “plugs” with concurrent replacement of smooth muscle wall and endothelium [3]. Uterine natural killer cells (NK) play critical roles in trophoblasts dependent spiral artery remodeling and the formation of endovascular trophoblastic “plugs” is associated with phenotypic switch of the endovascular trophoblasts to express CD56, a defining molecular marker for NK cell lineage [4,5,6,7,8]. During endometrial decidualization and subsequent embryonic/blastocyst implantation, estrogen, progesterone and human chorionic gonadotrophin (hCG) play critical roles in decidual, trophoblastic and fetal development, and the maintenance of pregnancy in the first trimester. Conclusion: WT1 potentially links the hormonal effects on endometrial decidualization and may play a role in gestational vascular transformation during pregnancy and restoration after pregnancy
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