Expression of Nemo-like kinase after spinal cord injury in rats

详细信息    查看全文

• 作者：Dawei Xu (1)
  Wei Zhao (2)
  Gang Pan (1)
  Ming Qian (2)
  Xinhui Zhu (1)
  Wei Liu (1)
  Gang Cai (1) (2)
  Zhiming Cui (1)
  
• 关键词：Nemo ; like kinase ; Apoptosis ; Signaling pathway ; Spinal cord injury
• 刊名：Journal of Molecular Neuroscience
• 出版年：2014
• 出版时间：March 2014
• 年：2014
• 卷：52
• 期：3
• 页码：410-418
• 全文大小：672 KB
• 作者单位：Dawei Xu (1)
  Wei Zhao (2)
  Gang Pan (1)
  Ming Qian (2)
  Xinhui Zhu (1)
  Wei Liu (1)
  Gang Cai (1) (2)
  Zhiming Cui (1)
  
  1. Department of Orthopedics, The Second Affiliated Hospital of Nantong University, Nantong, 226001, People’s Republic of China
  2. Department of Neurosurgery, The Second Affiliated Hospital of Nantong University, Nantong, 226001, People’s Republic of China
  
• ISSN：1559-1166

文摘

Wnt can induce signal transduction via the canonical pathway, which was involved in many processes in the nervous system. Nemo-like kinase (NLK) acts as a negative regulator of β-catenin/T-cell factor/lymphoid enhancer factor (LEF) and functions downstream of transforming growth factor β-activated kinase-1 in the Wnt signaling pathway. In this study, we performed a spinal cord injury (SCI) test in adult Sprague–Dawley rats and investigated the dynamic changes and role of NLK expression in the spinal cord. Western blot analysis revealed that NLK expression was low in normal spinal cord. It then increased markedly, peaked at 3?days, and declined to basal levels from 5?days after injury. Immunohistochemistry confirmed that NLK immunoactivity was expressed at low levels in gray and white matter under normal conditions and increased prominently in gray matter after the SCI test. Double immunofluorescent staining for NLK, caspase-3, β-catenin, and NeuN (neuronal nuclei) revealed that NLK and β-catenin were markedly increased and colocalized in apoptotic neurons. Coimmunoprecipitation data demonstrated that overexpression of NLK protein reduced β-catenin binding to LEF-1. Our results suggested that NLK was associated with neuronal apoptosis through attenuating the Wnt/β-catenin signaling pathway after SCIs.