APE1/ref1 gene provides anti-oxidative fate to Sca-1 positive cardiac progenitor cells and promotes cardiac repair via macrophage transition in ischemic environment
| Project/Area Number |
23618002
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Regenerative medicine
|
|---|
| Research Institution | Asahikawa Medical College |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
KAWABE Jun-ichi 旭川医科大学, 医学部, 特任准教授 (10400087)
HASEBE Naoyuki 旭川医科大学, 医学部, 教授 (30192272)
|
|---|
| Co-Investigator(Renkei-kenkyūsha) |
MATSUBARA Hiroaki (10239072)
|
|---|
| Project Period (FY) |
2011 – 2013
|
| Project Status |
Completed (Fiscal Year 2013)
|
| Budget Amount *help |
¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
|
|---|
| Keywords | Ape1 / 心筋再生 / 抗炎症 / 虚血耐性 / 細胞移植 / 抗酸化 / 炎症 / 血管新生 / 国際情報交換 / 再生医学 |
|---|
| Research Abstract |
The ROS production and apoptosis stimulated by H2O2 were significantly reduced in Ape1-CPCs compared with DsRed-CPCs. At 4 weeks, the absolute change in the LVEF was significantly greater in Ape1-CPCs injected mouse, but not DsRed-CPCs, than in the placebo group, that was associated with reduced infarcted size. Ape1-CPCs injected mouse were significantly enhanced the engraft cells compared with DsRed-CPCs injected mouse. In infarct myocardium of Ape1-CPCs injected mouse, M1 macrophages, but not M2 macrophages, were significantly reduced compared with that of DsRed-CPCs injected mouse. APE1/ref1 gene enhances the survival of engraft Sca1-CPC accompanied with the redox effect against oxidative stress in ischemic myocardium. Great survived Sca1-CPCs repaired the loss of LV function, which were associated with reduced infarcted myocardium and inflammation via macrophage transition. These results may provide an APE1/ref1 gene as a novel target to innovate the cardiac cell-therapy.
|
Report
(4 results)
Research Products
(2 results)
