| Project/Area Number |
26860139
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
General anatomy (including histology/embryology)
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| Research Institution | Juntendo University |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 低酸素 / 脳虚血 / 脳梗塞 / 神経細胞死 / Toll様受容体 / オートファジー / 炎症性サイトカイン / 海馬 |
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| Outline of Final Research Achievements |
Toll like receptors are one of the main contributors that induce inflammation under tissue injury and infection. We have previously reported that not only the excessive inflammation induced by TLR2, but also autophagy induction could aggravate disease states after neonatal hypoxic/ischemic (H/I) brain injury. Herein, we showed that the activation of TLR2 could directly induce autophagy after H/I injury. In contrast, the autophagy-impairment also revealed suppression of proinflammatory cytokine. Taken together, these data suggest that the activation of the TLR2-signaling pathway and autophagy induction leads to neuronal cell death in a synergistic action after neonatal-H/I brain injury.
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