| Project/Area Number |
15K10991
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Emergency medicine
|
|---|
| Research Institution | Wakayama Medical University |
|---|
Principal Investigator |
Ueda Kentaro 和歌山県立医科大学, 医学部, 講師 (20438279)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
木田 真紀 和歌山県立医科大学, 医学部, 講師 (00326381)
米満 尚史 和歌山県立医科大学, 医学部, 助教 (80382331)
|
|---|
| Project Period (FY) |
2015-04-01 – 2018-03-31
|
| Project Status |
Completed (Fiscal Year 2017)
|
| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2017: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
|---|
| Keywords | AKI / アポトーシス / オートファジー / Bcl-2遺伝子 / HGF遺伝子 / HVJ Envelope vector |
|---|
| Outline of Final Research Achievements |
First, Bcl-2 expression HVJ Envelope vector and HGF expression HVJ Envelope vector were prepared. These were transfected into M1 cells derived from renal cortical collecting duct cells and the effect of enhancing the expression of Bcl-2 or HGF was confirmed. We performed an in vivo experiment using the renal ischemia reperfusion model. In the group to which the Bcl-2 gene was administered, apoptosis and autophagy were clearly inhibited compared with the control group, and the deterioration of renal function was mild. Furthermore, by using HGF gene administration in combination therewith, it was possible to control almost even the AKI critically ill model.
|
