2022 Fiscal Year Final Research Report
Transcription factor WT1-mediated decidualization of endometrial stromal cells and regulation of lipid metabolism
Project/Area Number |
20K09645
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Review Section |
Basic Section 56040:Obstetrics and gynecology-related
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Research Institution | Yamaguchi University |
Principal Investigator |
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Project Period (FY) |
2020-04-01 – 2023-03-31
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Keywords | 子宮内膜間質細胞 / WT1 / 脂質蓄積 / VLDLR / 糖取り込み |
Outline of Final Research Achievements |
Wilms tumor 1 (WT1) regulates decidualization of human endometrial stromal cells (ESCs). Microarray analysis revealed that WT1 regulates many genes involved in lipid transport during decidualization. WT1 is involved in lipid accumulation (LA) during decidualization, and we identified very low-density lipoprotein receptor (VLDLR) as a factor downstream of WT1 that regulated.Furthermore, WT1 is involved in glucose uptake, and we identified glucose uptake by up-regulating glucose transporter 1 (GLUT1) as a factor downstream of WT1 that regulates glucose uptake. Taken together, WT1 is a transcription factor regulating lipid and glucose metabolism during decidualization in ESCs.
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Free Research Field |
生殖内分泌
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Academic Significance and Societal Importance of the Research Achievements |
我々は、転写因子WT1がヒト子宮内膜間質細胞の脱落膜化において脂質代謝制御のみならずグルコース代謝をも制御していることを世界で初めて同定した。着床過程において受精卵は脱落膜細胞層に浸潤し、この際に脱落膜化細胞は受精卵に栄養を渡す栄養供給源となるとも言われており、これは未だ十分に証明されていない着床機構の解明に大きく貢献するものであり価値のあることであると考えている。
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