| Research Collaborator |
FUJITA Tomoko 東京大学, 医学部附属病院, 特別研究員 (60375441)
HARAGUCHI Hirofumi 東京大学, 大学院医学系研究科, 大学院生
MATSUMOTO Leona 東京大学, 大学院医学系研究科, 大学院生
EGASHIRA Mahiro 東京大学, 農学生命科学研究科, 大学院生
MATSUO Mitsunori 東京大学, 大学院医学系研究科, 大学院生
HIRAOKA Takehiro 東京大学, 大学院医学系研究科, 大学院生
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| Budget Amount *help |
¥25,480,000 (Direct Cost: ¥19,600,000、Indirect Cost: ¥5,880,000)
Fiscal Year 2015: ¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2014: ¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2013: ¥6,500,000 (Direct Cost: ¥5,000,000、Indirect Cost: ¥1,500,000)
Fiscal Year 2012: ¥9,100,000 (Direct Cost: ¥7,000,000、Indirect Cost: ¥2,100,000)
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| Outline of Final Research Achievements |
It has been suggested that downregulation of progesterone signaling in the uterus is involved in the pathogenesis of preterm delivery. Based on mouse models of preterm birth and human decidual cell cuture system, we found that progesterone-induced gene expression pattern is markedly different between human decidual cells derived from women with and without preterm birth, and decidual p53-Sestrin-AMPK-mTORC1 pathway is a major pathway of preterm labor. These findings indicate that progesterone and mTOR pathways are possible therapeutic targets for preterm labor.
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