| Budget Amount *help |
¥17,160,000 (Direct Cost: ¥13,200,000、Indirect Cost: ¥3,960,000)
Fiscal Year 2017: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2016: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2015: ¥6,240,000 (Direct Cost: ¥4,800,000、Indirect Cost: ¥1,440,000)
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| Outline of Final Research Achievements |
The mean mRNA levels of both M1 and M2 markers in microglia acutely isolated from the hippocampus of wild-type mice were gradually and significantly increased after brain injury. In contrast, the mean mRNA levels of M1 markers in microglia acutely isolated from the hippocampus of cathepsin B-deficient mice showed no significant change after brain injury. The mean mRNA levels of the M2 markers increased rather rapidly to reach a peak after brain injury and then returned to the control level. Furthermore, cathepsin E-dependent proteasomal system is involved in an early activation of NF-kB in microglia after brain injury. Autophagy caused a delayed but long-lasting activation of NF-kB through cathepsin B-mediated autophagy machinery in microglia. Therefore, a proteolytic relay through modulator actions of cathepsins E and B could work as a phenotypic switch in microglia along the M1-M2 phenotypic continuum through the dynamics of NF-kB activity.
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