Project/Area Number |
20591874
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Urology
|
Research Institution | University of Fukui |
Principal Investigator |
AOKI Yoshitaka University of Fukui, 医学部, 助教 (30273006)
|
Co-Investigator(Kenkyū-buntansha) |
ITO Hideaki 福井大学, 医学部, 助教 (00345620)
YOKOYAMA Osamu 福井大学, 医学部, 教授 (90242552)
YOKOTA Yoshifumi 福井大学, 医学部, 教授 (50222386)
|
Project Period (FY) |
2008 – 2010
|
Project Status |
Completed (Fiscal Year 2010)
|
Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2010: ¥260,000 (Direct Cost: ¥200,000、Indirect Cost: ¥60,000)
Fiscal Year 2009: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2008: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
|
Keywords | 転写因子 / 腎盂尿管移行部狭窄 / 分化 / アンギオテンシン受容体 / SNP / 先天性尿路奇形 / 転写制御 / 水腎症 / 動物モデル |
Research Abstract |
We recently showed that Id2 mutant mice develop hydronephrosis with congenital obstruction at the ureteropelvic junction, the characteristics of which show a close resemblance to those of human congenital hydronephrosis. We investigated whether Id2 was involved in the pathogenesis of hydronephrosis using unilateral ureteral obstruction (UUO) mouse model. After 3 days of UUO, Id2 gene expressions of renal pelvis were increased by 2.4-fold. Ingenuity pathway Analysis and microarray expression data analysis from public data database suggested that Id2 gene related with Angiotensinogen.
|