2011年11月
c-Jun N-terminal kinase induces axonal degeneration and limits motor recovery after spinal cord injury in mice.
Neuroscience research
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- 巻
- 71
- 号
- 3
- 開始ページ
- 266
- 終了ページ
- 77
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.1016/j.neures.2011.07.1830
- 出版者・発行元
- 3
c-Jun N-terminal kinase (JNK) mediates neuronal death in response to stress and injury in the CNS and peripheral nervous system. Here, we show that JNK also regulates retrograde axonal degeneration (axonal dieback) after spinal cord injury (SCI) in mice. Activated phospho-JNK was highly expressed in damaged corticospinal tract (CST) axons after thoracic SCI by hemisection. Local administration of SP600125, a JNK inhibitor, prevented accumulation of amyloid-β precursor protein and retraction of the severed CST axons as well as preserved the axonal arbors rostral to the injury site. The treatment with SP600125 also improved functional recovery of the hindlimbs, assessed by Basso mouse scale open-field scores and the grid-walking test. In Jnk1(-/-) and Jnk3(-/-) mice, we observed prevention of axonal degeneration and enhancement of motor recovery after SCI. These results indicate that both JNK1 and JNK3 induce axonal degeneration and limit motor recovery after SCI. Thus, a JNK inhibitor may be a suitable therapeutic agent for SCI.
- リンク情報
- ID情報
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- DOI : 10.1016/j.neures.2011.07.1830
- ISSN : 0168-0102
- CiNii Articles ID : 80022070864
- PubMed ID : 21824499