Abstract
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 3days, and declined to basal levels from 5days 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.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
