| Project/Area Number |
24890214
|
|---|
| Research Category |
Grant-in-Aid for Research Activity Start-up
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Functional basic dentistry
|
|---|
| Research Institution | Saitama Medical University (2013)
Kyushu Dental College (2012) |
|---|
Principal Investigator |
OSAWA Kenji 埼玉医科大学, 医学部, 助教 (70638238)
|
|---|
| Project Period (FY) |
2012-08-31 – 2014-03-31
|
| Project Status |
Completed (Fiscal Year 2013)
|
| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
|---|
| Keywords | 骨代謝 / 骨吸収 / 破骨細胞 / 細胞内情報伝達 / p130Cas / c-Src / Integrin / p130 Cas |
|---|
| Research Abstract |
Osteoclast-specific p130Cas conditional knockout mice (p130Cas cKO) exhibit a high bone mass phenotype caused by defect in multinucleation and cytoskeleton organization causing bone resorption deficiency. Bone marrow cells from p130Cas cKO were able to differentiate into osteoclasts and wild-type cells in vitro. However, osteoclasts from p130Cas cKO failed to form actin rings and resorb pits on dentine slices. Although the initial events of osteoclast attachment were intact, the Rac1 activity that organizes the actin cytoskeleton was reduced, and its distribution was disrupted in p130Cas cKO osteoclasts. Dedicator of cytokinesis 5 (Dock5), a Rho family guanine nucleotide exchanger, failed to associate with Src or Pyk2 in osteoclasts in the absence of p130Cas. These results strongly indicate that p130Cas plays pivotal roles in osteoclastic bone resorption
|
