| Project/Area Number |
10670591
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Neurology
|
|---|
| Research Institution | Saga Medical School |
|---|
Principal Investigator |
KURODA Yasuo Saga Medical School, Department of Medicine, Professor, 医学部, 教授 (30117105)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
SATOH Junichi Saga Medical School, Department of Medicine, Lecturer, 医学部, 講師 (30274591)
|
|---|
| Project Period (FY) |
1998 – 2000
|
| Project Status |
Completed (Fiscal Year 2000)
|
| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2000: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1999: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1998: ¥1,500,000 (Direct Cost: ¥1,500,000)
|
|---|
| Keywords | prion / astrocyte / heat-shock protein / gene expression / プリオン病 / Ras / Rac1シグナル伝達 / 神経細胞 / サイトカイン / TNF-α / IL-1β |
|---|
| Research Abstract |
We have previously shown that astrocyte-derived cytokines could modify the expression of prion protein (PrP) gene in the cultured human neuronal cells. In order to clarify the influence of modified PrP metabolism on cell functions, we investigated expressions of heat-shock protein genes and Ras/Racl genes in PrP gene-knock out mice and normal control mice. We studied 7 major heat-shock protein genes but could not find differences in their expression between PrP-knock out mice and the controls However, we found the significant down-regulation of genes of RTK, Eps8 and CD44 in the PrP-knock out mice when compared to the controls. These results suggest a possibility that astrocyte-derived cytokines may cause neuronal degeneration by modifing PrP metabolism which can cause down-regulation of Ras/Racl intracellular signal system.
|
