Molecular mechanism of gender dependent difference in the neural tube defect manifestation.
Project/Area Number |
20591297
|
Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Embryonic/Neonatal medicine
|
Research Institution | Tottori University |
Principal Investigator |
NARUSE Ichiro Tottori University, 医学部, 教授 (20113326)
|
Co-Investigator(Kenkyū-buntansha) |
UETA Etsuko 鳥取大学, 医学部, 講師 (40335526)
|
Project Period (FY) |
2008 – 2010
|
Project Status |
Completed (Fiscal Year 2010)
|
Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2008: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
Keywords | 先天異常 / 脳神経疾患 / 催奇形性 / 性差 / Gli3 / オクラトキシン / マイクロアレイ |
Research Abstract |
Prevalence of neural tube defects (NTDs) is larger in female in human. Pdn/Pdn mouse, whose responsible gene is Gli3, has a 16% risk of NTDs, and confines in female. When Ochratoxin A (OTA) was exposed to Pdn/Pdn mouse embryo, only male Pdn/Pdn manifested increased incidence of NTDs. After exposure to OTA on day 7.5 of gestation, Daam, Hoxbl, Tbx, Hmx3, Dlxl, Tlxh gene expressions were severely up-regulated in the +/+ and Pdn/Pdn embryos on day 9 of gestation. Ectopic expressions of Fgf8 and Emx2 were observed in the OTA-treated Pdn/Pdn embryos. From these investigations, it was speculated that NTDs manifestation is induced by the altered multiple gene expressions.
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Report
(4 results)
Research Products
(24 results)