| Project/Area Number |
16K10581
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Digestive surgery
|
|---|
| Research Institution | Kitasato University |
|---|
Principal Investigator |
ITO YOSHIYA 北里大学, 医学部, 講師 (40203187)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
隈元 雄介 北里大学, 医学部, 教授 (20596431)
|
|---|
| Project Period (FY) |
2016-04-01 – 2019-03-31
|
| Project Status |
Completed (Fiscal Year 2018)
|
| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
|---|
| Keywords | 肝 / 再生 / 修復 / プロスタグランジン / プロスタノイド / 免疫細胞 / 肝修復 / 脂質 / 肝再生 |
|---|
| Outline of Final Research Achievements |
Although liver repair is determinant for the patients underwent liver surgery, the underlying mechanisms of liver repair remain still unclear. In this study, we examined the role of prostaglandin (PG) E2 in liver repair using genetic mice. mPGES-1 deficient mice exhibited enhancement of liver repair after hepatic ischemia reperfusion through recruitment of repair macrophages. Concomitantly, the inhibitor for mPGES-1 facilitated liver repair. Among four PGE receptor subtypes, EP4 signaling was involved in delay in liver repair, and EP3 signaling contributed to promotion of liver repair. In addition, hepatic dendritic cells were accumulated into the liver during repair phase of hepatic ischemia reperfusion injury through EP3 signaling.
|
| Academic Significance and Societal Importance of the Research Achievements |
生理活性脂質であるプロスタグランジンが、肝障害後の炎症収束や修復に積極的な役割を果たしていることが明らかになる。修復マクロファージに分化していく過程に生理活性脂質を介した樹状細胞の関与とその制御機構をさらに解明することによって、肝再生治療に応用できる可能性がある。
|
