Project/Area Number |
24591856
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Radiation science
|
Research Institution | National Institute of Radiological Sciences |
Principal Investigator |
NAKAYAMA Fumiaki 独立行政法人放射線医学総合研究所, 重粒子医科学センター, チームリーダー (50277323)
|
Co-Investigator(Renkei-kenkyūsha) |
IMAI Takashi 独立行政法人放射線医学総合研究所, 重粒子医科学センター, プログラムムリーダー (50183009)
|
Research Collaborator |
UMEDA Sachiko
|
Project Period (FY) |
2012-04-01 – 2015-03-31
|
Project Status |
Completed (Fiscal Year 2014)
|
Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
Keywords | 放射線障害 / 防護剤 / 治療薬 / 増殖因子 / 再生医療 / 蛋白質 / 放射線 / 細胞内移行 / 再生医学 / 生体分子 |
Outline of Final Research Achievements |
FGF12 can be internalized into cells using two domains (CPP-M, CPP-C). This study aimed at clarifying the role of FGF12 internalization in protection against radiation-induced intestinal injury. Administration of FGF12 into BALB/c mice after radiation exposure was as effective as pretreatment in significantly promoting intestinal regeneration from radiation damage. Two domains, comprising amino acid residues 80-109 and 140-169 of FGF12B, were identified as being responsible for the radioprotective activity. Interestingly, these regions included the CPP-M and CPP-C domains, respectively; however, CPP-C by itself did not show an anti-apoptotic effect. In addition, internalized FGF12 suppressed the activation of p38α after irradiation, resulting in reduced radiation-induced apoptosis. These findings indicate that FGF12 can protect the intestine against radiation-induced injury through its internalization, independently of FGFRs.
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