Project/Area Number |
20591928
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Obstetrics and gynecology
|
Research Institution | Saitama Medical University |
Principal Investigator |
KAJIHARA Takeshi Saitama Medical University, 医学部, 准教授 (80286103)
|
Co-Investigator(Kenkyū-buntansha) |
ISHIHARA Osamu 埼玉医科大学, 医学部, 教授 (70176212)
ITAKURA Atsuo 埼玉医科大学, 医学部, 教授 (70262897)
|
Project Period (FY) |
2008 – 2010
|
Project Status |
Completed (Fiscal Year 2010)
|
Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2010: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2009: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2008: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
|
Keywords | 子宮内膜脱落膜化 / 子宮内膜 / 脱落膜化 / SOD2 / 酸化ストレス / HCG / ヒト子宮内膜間質細胞 / フォークヘッド転写因子 / hCG |
Research Abstract |
To test this hypothesis, primary HESCs cultures were decidualized with 8-bromo-cAMP and medroxyprogesterone acetate in the presence or absence of rhCG at various concentrations. Hydrogen peroxide was used as a source of reactive oxygen species (ROS). rhCG conferred additional protection to oxidative cell death in decidualizing HESCs in a dose-dependent manner. In parallel, rhCG augmented the expression of the decidual transcription factor FOXO1 and its downstream target, the ROS scavenger superoxide dismutase 2 (SOD2). These results suggest that hCG improves the uterine environment upon implantation by suppressing apoptotic responses the maternal decidua under oxidative stress conditions.
|