Journal
EUROPEAN NEUROLOGY
Volume 81, Issue 3-4, Pages 197-204Publisher
KARGER
DOI: 10.1159/000502004
Keywords
Spinal cord injury; Wnt-3a; Wnt/beta-catenin signaling pathway; Neuroprotection; Axon regeneration; Autophagy; Apoptosis; Mammalian target of rapamycin signaling pathway
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Funding
- National Natural Science Foundation of China [81801906]
- Natural Science Foundation of Shandong [ZR2018PH024, ZR2015YL034]
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Background: Spinal cord injury (SCI) is a constant challenge in medical research and a global therapeutic problem. Treatment of this condition remains difficult in clinical practice. Hence, prevention, treatment, and rehabilitation of SCI have become imminent tasks in the medical field. Summary: Recent evidence suggest the important role of Wnt/beta-catenin signaling pathway, a canonical Wnt signaling pathway, in neural development, axon guidance, neuropathic pain relief, and neuronal survival. Wnt-3a is regarded as an activator of the canonical Wnt signaling pathway. This activator is expressed in the dorsal midline region and is responsible for spinal cord development. In addition, Wnt-3a plays a regulatory role in autophagy, apoptosis, and regeneration of neurons; neurogenic inflammation; and axon regeneration. Herein, we demonstrated that neuronal autophagy was regulated by Wnt-3a via beta-catenin and mammalian target of rapamycin signaling pathways after SCI. Our study also discovered that the Wnt-3a provided a favorable microenvironment for the recovery of nerve function after SCI. Key Messages: This study systematically elaborates the neuroprotective effect of Wnt-3a and its neuroprotection molecular mechanism after SCI. This study provides a new molecular mechanism and research basis for clinical treatment of SCI. (C) 2019 S. Karger AG, Basel
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