Elucidation of the mechanism of promotion of vascular intimal thickening by bone marrow-derived cells using Epac1-deficient mice
| Project/Area Number |
17K08976
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Laboratory medicine
|
|---|
| Research Institution | Tokyo Medical University (2020)
Tokyo Medical and Dental University (2017-2019) |
|---|
Principal Investigator |
Kato Yuko 東京医科大学, 医学部, 講師 (50580875)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
横山 詩子 東京医科大学, 医学部, 主任教授 (70404994)
|
|---|
| Project Period (FY) |
2017-04-01 – 2021-03-31
|
| Project Status |
Completed (Fiscal Year 2020)
|
| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
|---|
| Keywords | 血管内膜肥厚 / 血管平滑筋細胞 / 骨髄由来細胞 / 骨髄由来前駆細胞 / Epac1 |
|---|
| Outline of Final Research Achievements |
In this study, we clarified the mechanism of intimal thickening by focusing on Exchange protein directly activated by cyclic AMP 1 (Epac1), a signaling molecule that promotes intimal thickening. The effect of bone marrow-derived cells on the formation of intimal thickening was limited, and Epac1 was thought to be involved in the formation of intimal thickening by acting on cells derived from vascular tissue rather than bone marrow-derived cells. Furthermore, Epac1 is involved in the Akt/GSK3β-mediated signaling pathway that is activated by basic fibroblast growth factor, which is important for the formation of intimal thickening after vascular injury, suggesting that Epac1 is involved in the promotion of intimal thickening.
|
| Academic Significance and Societal Importance of the Research Achievements |
一般に虚血性心疾患患者に対して行われる経皮的冠動脈形成術では、施術により損傷した血管組織の治癒過程で血管内膜肥厚が起こる。約40％の患者ではこの血管内膜肥厚が過剰となり、血管の再狭窄や閉塞を起こす。現在臨床ではこれらを抑制するための薬剤流出ステントが使用されているものの、遅発性の血栓症など別の問題が発生しており、別の新しい治療法の開発が望まれている。本研究で明らかにした血管内膜肥厚形成の新しいメカニズムは血管再狭窄を抑制する新しい治療法を提案する基盤となると考えられる。
|
Report
(5 results)
Research Products
(7 results)
