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Journal of Huazhong University of Science and Technology (Medical Sciences) ; (6): 548-553, 2016.
Article in English | WPRIM | ID: wpr-285231

ABSTRACT

Evidence suggested that glycogen synthase kinase-3β (GSK-3β) is involved in Nogo-66 inhibiting axonal regeneration in vitro, but its effect in vivo was poorly understood. We showed that stereotactic injection of shRNA GSK-3β-adeno associated virus (GSK-3β-AAV) diminished syringomyelia and promoted axonal regeneration after spinal cord injury (SCI), using stereotactic injection of shRNA GSK-3β-AAV (tested with Western blotting and RT-PCR) into the sensorimotor cortex of rats with SCI and by the detection of biotin dextran amine (BDA)-labeled axonal regeneration. We also determined the right position to inject into the sensorimotor cortex. Our findings consolidate the hypothesis that downregulation of GSK-3β promotes axonal regeneration after SCI.


Subject(s)
Animals , Humans , Rats , Axons , Metabolism , Dependovirus , Genetics , Glycogen Synthase Kinase 3 beta , Genetics , Metabolism , Nerve Regeneration , Genetics , RNA, Small Interfering , Genetics , Sensorimotor Cortex , Pathology , Spinal Cord Injuries , Genetics , Pathology , Therapeutics , Syringomyelia , Genetics , Pathology , Therapeutics
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