Project/Area Number |
19390288
|
Research Category |
Grant-in-Aid for Scientific Research (B)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Pediatrics
|
Research Institution | Keio University |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
UCHIDA Keiko 慶應義塾大学, 医学部, 共同研究員 (50286522)
YAMAGISHI Chihiro 慶應義塾大学, 医学部, 共同研究員 (10296618)
MAKINO Shinji 慶應義塾大学, 医学部, 准教授 (20306707)
|
Project Period (FY) |
2007 – 2009
|
Project Status |
Completed (Fiscal Year 2009)
|
Budget Amount *help |
¥18,330,000 (Direct Cost: ¥14,100,000、Indirect Cost: ¥4,230,000)
Fiscal Year 2009: ¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2008: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2007: ¥7,670,000 (Direct Cost: ¥5,900,000、Indirect Cost: ¥1,770,000)
|
Keywords | 小児循環器学 / 形態形成 / 細胞分化 / 分子生物学 / 発生医学 / 疾患モデル動物 / シグナル伝達 |
Research Abstract |
Intracellular calcium signaling is known to play essential roles in cardiac physiology and hypertrophy, however, its function in cardiac development remains to be elucidated. Inositol 1,4,5-trisphosphate receptors (IP_3R type1, 2 and 3) are intracellular calcium release channels on the endo/sarcoplasmic reticulum. IP_3R1, 2 double knockout mouse (DKO) embryos and IP_3R1, 3 DKO embryos died around E10.5 with signs of heart failure while each single knockout mouse showed normal cardiogenesis. In the IP_3R1, 2 DKO embryos, the atrioventricular cushion development was impaired involving the NFATc signal, whereas the outflow tract development, implicated in the second heart field, was affected in the IP_3R1, 3 DKO embryos. This research project revealed that intracellular calcium signaling redundantly mediated by three subtypes of IP_3R may play a role in development of each specific module of cardiovascular development.
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