| Project/Area Number |
18K09037
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Review Section |
Basic Section 56020:Orthopedics-related
|
|---|
| Research Institution | Kagoshima University |
|---|
Principal Investigator |
Yamamoto Takuya 鹿児島大学, 医歯学総合研究科, 客員研究員 (40381157)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
廣津 匡隆 鹿児島大学, 医歯学域鹿児島大学病院, 講師 (00444901)
瀬戸口 啓夫 鹿児島大学, 医歯学総合研究科, 客員研究員 (40423727)
|
|---|
| Project Period (FY) |
2018-04-01 – 2021-03-31
|
| Project Status |
Completed (Fiscal Year 2020)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2020: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2019: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2018: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
|
|---|
| Keywords | 神経障害性疼痛 / TGF-beta / ミクログリア / TGF-β / 慢性疼痛 / 腸内細菌 / 腸内細菌叢 |
|---|
| Outline of Final Research Achievements |
The activation and proliferation of microglia is characteristic of the early stages of brain pathologies. In this study, we aimed to identify a factor that promotes microglial activation and proliferation and examined the in vitro effects on these processes. The results showed that only transforming growth factor beta (TGF-β) caused an increase in the in vitro proliferation of both microglial cell lines.In addition, a TGF-β receptor 1 inhibitor, galunisertib, caused marked inhibition of proliferation in a dose-dependent manner, indicating that inhibition of TGF-β signalling reduces the proliferation of microglia. Therefore, galunisertib may represent a promising therapeutic agent for the treatment of neurodegenerative diseases via inhibition of nerve injury-induced microglial proliferation, which may result in reduced inflammatory and neuropathic and cancer pain.
|
| Academic Significance and Societal Importance of the Research Achievements |
神経障害性疼痛に悩まされている患者は多い。しかし、神経障害性疼痛の治療は困難で、その治療法の開発は社会的に有意義である。神経障害性疼痛の原因のひとつにミクログリアの異常増殖があることが知られている。我々はミクログリアは TGF-beta1で増殖が亢進し、TGF-beta1のシグナルを制御することが、慢性疼痛の治療に応用できることを示した。これらは新規治療法開発の一助となる研究成果である。
|
