Autophagy disruption by sugar chain in injury neurons
Project/Area Number |
16K21083
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Neurophysiology / General neuroscience
Nerve anatomy/Neuropathology
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Research Institution | Nagoya University |
Principal Investigator |
Ozaki Tomoya 名古屋大学, 医学系研究科, 助教 (40710588)
|
Project Period (FY) |
2016-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2017: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
Keywords | コンドロイチン硫酸プロテオグリカン / 糖鎖 / dystrophic growth cone / オートファジー中断 / 軸索再生 / 脊髄損傷 / 軸索再伸長阻害 / オートファジー |
Outline of Final Research Achievements |
Our research analyzed hallmark of injury axon dystrophic growth cone and its formation. This study demonstrated that (i) autophagosomes accumulate in the dystrophic growth cone in vivo injury spinal cord of mouse, (ii) The formation of dystrophic growth cone was induced by gene knockdown of SNARE proteins which work at fusion step between autophagosomes and lysosomes in autophagic flux and (iii) chemically synthetized sugar chain or some compounds can rescue dystrophic growth cone cultured on chondroitin sulfate proteoglycan gradient. These result suggest autophagy as treatment target to axon regeneration failure.
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Report
(3 results)
Research Products
(10 results)