| 研究実績の概要 |
Reproductive aging implies a sharp decline in female fertility and an increase in pregnancy complications with maternal age. The major characteristics of reproductive aging are low birth rate/embryonic malformation caused by defective decidualization at early pregnancy, and prolong gestational period at late pregnancy. At early pregnancy, progesterone at a specific level is required to induce successful endometrial decidualization, while in late pregnancy progesterone withdrawal from myometrium is mandatory for starting myometrial contraction and on-time delivery. A higher level of progesterone than optimal during early or late pregnancy reported to cause defective decidualization as well as delayed delivery, respectively. In aged female mice, we observed a minor change in Estrogen but higher progesterone levels than young mice in early pregnancy with no progesterone withdrawal at late pregnancy, which can be the cause of the defective decidualization and the long gestation. The defective homeostasis of progesterone levels in aged females has not been characterized yet. This year, I cleared the molecular mechanisms controlling normal progesterone levels during early and late stages of pregnancy.
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| 今後の研究の推進方策 |
I am planing to The downstream targets of progesterone causing the abnormal physiological status during pregnancy. As a preliminary result, we found a Class II Basic Helix-Loop-Helix protein (TCF23) deletion in 6M old mice showed an abnormal/inflamed uterine decidua and obstructed labor, which might indicate its role as negative regulator of progesterone. The output of the current project will support maintaining suitable strategies of caring an aged woman during pregnancy, which is a burgeoning clinical problem.
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