| Project/Area Number |
21591383
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Pediatrics
|
|---|
| Research Institution | Tokyo Women's Medical University (2011)
The University of Tokyo (2009-2010) |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
TOMITA Sachiko 東京女子医科大学, 医学部, 助教 (40231451)
ISO Naoyuki 東京大学, 医科学研究所, 助教 (80420214)
|
|---|
| Project Period (FY) |
2009 – 2011
|
| Project Status |
Completed (Fiscal Year 2011)
|
| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2010: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2009: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
|
|---|
| Keywords | 発生学・形態形成学 / 先天異常学・奇形学 / 心血管 / 発生 / 分化 / バーシカン / 循環器・高血圧 |
|---|
| Research Abstract |
The expression of the Cspg2 gene, which encodes the extracellular matrix protein, versican, is disrupted in the heart defect(hdf) mouse. Therefore, the hdf mouse is a good model to examine the function of Cspg2 gene in embryonic cardiovascular development. The vascular formation was disrupted particularly at the dorsal region of the hdf embryos and that the second heart field segment was diminished in hdf embryos. The initial delamination of the neural crest from the neural tube epithelium appeared to be normal, however, the transformed neural crest cells were disrupted in hdf mouse embryos. Versican, may protect cephalic mesenchyme from massive apoptosis, thereby contributing to the neural crest cells and the cells in second heart field.
|
