| Project/Area Number |
15K10658
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Obstetrics and gynecology
|
|---|
| Research Institution | Gunma University |
|---|
Principal Investigator |
ABE Yumiko 群馬大学, 大学院保健学研究科, 准教授 (70261857)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
峯岸 敬 群馬大学, その他部局等, 理事 (00209842)
|
|---|
| Project Period (FY) |
2015-04-01 – 2018-03-31
|
| Project Status |
Completed (Fiscal Year 2017)
|
| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2017: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
|
|---|
| Keywords | 羊膜細胞 / アクチビン / インヒビン / フォリスタチン / FSTL-3 / FIRS / 絨毛膜羊膜炎 / 炎症性サイトカイン / TNF-α / IL-1β |
|---|
| Outline of Final Research Achievements |
Fetal Inflammatory Response Syndrome (FIRS) develops when inflammation extends to the amnion and the umbilical cord in chorioamnionitis. The survival rate is reported to increase in experimental animals with sepsis as a result of the administration of an activin binding protein which negates the activity of activin. Therefore, we studied the effects of inflammatory cytokines on the synthesis of activin and negative regulators of activin in human amniotic cells. Inflammatory cytokines predominantly stimulated the synthesis of activin compared to that of negative regulators of activin. Some of the signal transduction pathways involved in increased activin synthesis by the inflammatory cytokine TNF-alpha were also elucidated in this study. From these results, the inhibition of the synthesis of activin in human amniotic cells and the administration of negative regulators of activin appear to be exploitable for the development of a new FIRS therapy.
|
