| Budget Amount *help |
¥127,400,000 (Direct Cost: ¥98,000,000、Indirect Cost: ¥29,400,000)
Fiscal Year 2015: ¥20,410,000 (Direct Cost: ¥15,700,000、Indirect Cost: ¥4,710,000)
Fiscal Year 2014: ¥23,140,000 (Direct Cost: ¥17,800,000、Indirect Cost: ¥5,340,000)
Fiscal Year 2013: ¥24,440,000 (Direct Cost: ¥18,800,000、Indirect Cost: ¥5,640,000)
Fiscal Year 2012: ¥24,180,000 (Direct Cost: ¥18,600,000、Indirect Cost: ¥5,580,000)
Fiscal Year 2011: ¥35,230,000 (Direct Cost: ¥27,100,000、Indirect Cost: ¥8,130,000)
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| Outline of Final Research Achievements |
A disruption of intercellular communications among glial cells and neuron after nerve injury leads to neuronal death. We have examined molecules, which mediate interactions between glial cells and injured neurons. We have identified that DINE (damage induced neuronal endopeptidase) and PAP-III/RegIII-g (an inflammatory associated lectin-like protein) are implicated in neuron-Schwann cell interactions during nerve regeneration and development. In addition we have proved that DAP12, which is expressed by microglia, prolongs inflammatory response and is a exacerbating signal for injured motor neurons. We also succeeded in making BAC transgenic mouse Tg(ATF3-mtGPF/Cre), which expresses Cre and mitochondria localizing GFP under ATF3 promoter. This could be a useful tool for future analysis in our project as well as collaborations with other members in A01, A02 and A03.
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