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Beta-nerve growth factor gene therapy alleviates pyridoxine-induced neuropathic damage by increasing doublecortin and tyrosine kinase A in the dorsal root ganglion

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Neural Regeneration Research 2020年第1期15卷 162-168页

作者： Hyun-Kee Cho Woosuk Kim Kwon-Young Lee Jin-Ok Ahn Jung Hoon Choi In Koo Hwang Jin-Young Chung Department of Veterinary Internal Medicine and Institute of Veterinary Science College of Veterinary MedicineKangwon National UniversityChuncheonKangwon-doSouth Korea Department of Anatomy and Cell Biology College of Veterinary MedicineResearch Institute for Veterinary ScienceSeoul National UniversitySeoulSouth Korea Department of Anatomy College of Veterinary MedicineKangwon National UniversityChuncheonKangwon-doSouth Korea

Beta-nerve growth factor(β-NGF)is known to be a major leading cause of neuronal plasticity.To identify the possible action mechanisms ofβ-NGF gene therapy for sciatic nerve recovery,experimental dogs were randomly divided into control,pyridoxine,and pyridoxine+β-NGF groups.We observed chronological changes of morphology in the dorsal root ganglia in response to pyridoxine toxicity based on cresyl violet staining.The number of large neurons positive for cresyl violet was dramatically decreased after pyridoxine intoxication for 7 days in the dorsal root ganglia and the neuron number was gradually increased after pyridoxine withdrawal.In addition,we also investigated the effects ofβ-NGF gene therapy on neuronal plasticity in pyridoxine-induced neuropathic dogs.To accomplish this,tyrosine kinase receptor A(TrkA),βIII-tubulin and doublecortin(DCX)immunohistochemical staining was performed at 3 days after the last pyridoxine treatment.TrkA-immunoreactive neurons were dramatically decreased in the pyridoxine group compared to the control group,but strong TrkA immunoreactivity was observed in the small-sized dorsal root ganglia in this group.TrkA immunoreactivity in the dorsal root ganglia was similar betweenβ-NGF and control groups.The numbers ofβⅢ-tubulin-and DCX-immunoreactive cells decreased significantly in the pyridoxine group compared to the control group.However,the reduction ofβⅢ-tubulin-and DCX-immunoreactive cells in the dorsal root ganglia in theβ-NGF group was significantly ameliorated than that in the pyridoxine group.These results indicate thatβ-NGF gene therapy is a powerful treatment of pyridoxine-induced neuropathic damage by increasing the TrkA and DCX levels in the dorsal root ganglia.The experimental protocol was approved by the Institutional Animal Care and Use Committee(IACUC)of Seoul National University,South Korea(approval No.SNU-060623-1,SNU-091009-1)on June 23,2006 and October 9,2009,respectively.

关键词： β-nerve growth factor βⅢ-tubulin doublecortin gene therapy neuron-glial antigen 2 neuropathy pyridoxine

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