Progesterone resistance and it molecular targets in preterm birth

2015 Fiscal Year Final Research Report

• Project/Area Number: 24689062
• Research Category: Grant-in-Aid for Young Scientists (A)
• Allocation Type: Partial Multi-year Fund
• Research Field: Obstetrics and gynecology
• Research Institution: The University of Tokyo
• Principal Investigator: Hirota Yasushi 東京大学, 医学部附属病院, 講師 (40598653)
• 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
• Project Period (FY): 2012-04-01 – 2016-03-31
• Keywords: 早産 / マウスモデル / ヒト初代培養細胞 / 脱落膜 / mTOR / プロゲステロン / p53

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.

Free Research Field

産婦人科学