Mechanisms by which C/EBPb inducues genome-wide H3K27ac during decidualization of human endometrial stromal cells

2020 Fiscal Year Final Research Report

• Project/Area Number: 18K09230
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 56040:Obstetrics and gynecology-related
• Research Institution: Yamaguchi University
• Principal Investigator: TAMURA Isao 山口大学, 医学部附属病院, 助教 (40610663)
• Project Period (FY): 2018-04-01 – 2021-03-31
• Keywords: 子宮内膜 / 脱落膜化 / epigenetics / C/EBPb / PGC-1a

Outline of Final Research Achievements

C/EBPb regulates the expression of many decidualization-related genes through the genome-wide regulation of H3K27ac modification. In this study, we aimed to elucidate the detailed mechanism by which C/EBPb induces H3K27ac. We found that C/EBPb up-regulates the expression of PGC1a, which is an epigenetic transcription factor. In addition, C/EBPb forms a complex with PGC-1a and p300 to induce H3K27ac. Although the role of PGC-1a in the human endometrium has been unclear, our study demonstrated that PGC-1a contributes to decidualization by inducing epigenomic changes. Furthermore, PGC-1a may be involved in the immune regulation during decidualization.

Free Research Field

生殖内分泌学

Academic Significance and Societal Importance of the Research Achievements

本研究により子宮内膜間質細胞における遺伝子発現調節機構の一つが明らかとなった。脱落膜化は着床現象に必須の事象である。よって、本研究により脱落膜化の調節機構のひとつが明らかとなり、未だ詳細が不明であるヒト着床現象の解明につながると考えられる。このことは将来の不妊症治療にもつながるため、社会的意義がある研究である。