During implantation, endometrial cells undergo functional and structural changes, and support the successful embryo development. This reaction is known as decidualization and is critical to placental formation and to prevent the uterine functions. This progress is achieved by complex communication of regulators such as hormones, cytokines and growth factors. Some of the TGF-b superfamily members such as inhibin, activin, TGF-β, and bone morphogenetic proteins (BMP) involve in uterine modulation during pregnancy. Müllerian inhibiting factor (MIF) is a member of TGF-β superfamily and regulate folliculogenesis, but its expression and roles in uterus are not clear. In this study, we investigated the expression of MIF and its receptor Ⅱ in decidualizing endometrium. Interestingly its expression was detected in the fully decidualized cells. Its receptor II was detected in undifferentiated stromal cells. MIF expression was increased by decidual maturation and MIF receptor II was decreased by decidual reaction. MIF expression was induced by estrogen and its receptor II was increased by only progesterone in the stroma cells primed with estrogen. In the uterus of delayed implantation model mice, MIF expression was peak after 6 hr of estrogen administration. MIF receptor II expression was not induced. It means that MIF and MIF receptor II are expressed in the stroma cells with the specificity on physiological status. Based on them, it is suggested that MIF may work as paracrine factors in uterus during decidualization.

• Eunbee Joe(Division of Developmental Biology and Physiology, Sungshin Women’s University)
• Mi Hee Oh(Division of Developmental Biology and Physiology, Sungshin Women’s University)
• Hyun Tae Park(Department of Obstetrics and Gynecology, Korea University Anam Hospital)
• Yong-Pil Cheon(Division of Developmental Biology and Physiology, Sungshin Women’s University)