| Project/Area Number |
21591907
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Orthopaedic surgery
|
|---|
| Research Institution | Tokai University |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
SUYAMA Kaori 東海大学, 医学部, 助教 (20433914)
|
|---|
| Project Period (FY) |
2009 – 2011
|
| Project Status |
Completed (Fiscal Year 2011)
|
| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2011: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2009: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
|
|---|
| Keywords | 脊椎脊髄病学 / 脊髄損傷 / 二次損傷 / オリゴデンドロサイト前駆細胞 / アポトーシス / 小胞体ストレス / GRP78 / CHOP/GADD153 / オリゴデンドロサイト / 再髄鞘化 |
|---|
| Research Abstract |
In this study, We focused on endoplasmic reticulum(ER) stress as a cause of apoptosis of oligodendrocyte precursor cell(OPC) following spinal cord injury, and examined it in vivo, and in vitro. In addition, We investigated the effects of G-CSF and SCF on intrinsic cells, and motor function recovery in spinal cord-injured mice. The results showed that the combined administration of SCF and G-CSF in mouse contusive spinal cord injury model not only improved motor function, but also induced the accumulation of intrinsic microglia and the active proliferation of intrinsic OPC. Our results suggest that apoptosis by the ER stress is involved in the differential inhibition of OPC, and To increase the tolerance of ER stress response of OPC may result in remyelination of damaged spinal cord.
|
