ArticleMedical science monitor : international medical journal of experimental and clinical research2017
Differential Expression of Tubulin Acetylase and Deacetylase Between the Damaged Central and Peripheral Branch of Dorsal Root Ganglion Neurons.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- Unleashing Axonal Regeneration Capacities: Neuronal and Non-neuronal Changes After Injuries to Dorsal Root Ganglion Neuron Central and Peripheral Axonal Branches.Molecular neurobiology · 2024Review
- Overexpression of SIRT2 Alleviates Neuropathic Pain and Neuroinflammation Through Deacetylation of Transcription Factor Nuclear Factor-Kappa B.Inflammation · 2018Article
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2 authors at 1 institution in 1 country.
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Abstract
BACKGROUND The differences between the peripheral and central branches of the dorsal root ganglion (DRG) have not been fully elucidated. This study aimed to explore the expression of tubulin post-translational modifications (acetylation and deacetylation) between damaged peripheral and central branches of DRG neurons. MATERIAL AND METHODS Fifty Sprague-Dawley rats were randomly assigned to five groups with 10 rats in each group. These five groups consisted of spinal nerve ligation (SNL) at 24 hour and 48 hour, and cauda equina compression (CEC) at 24 hour and 48 hour, and a sham group. SNL injury in rats was induced by ligating L5 and L6 spinal nerves with 1-0 silk thread outboard the DRGs. CEC injury in rats was induced by a piece of silicone (10×1×1 mm) placed under the laminae of the L5-6 vertebra. Sham-operated rats underwent a simple laminectomy in L4, but silicone was not implanted. The expression profile of acetylase and deacetylase was examined by real-time PCR, Western blotting, and immunohistochemistry. RESULTS In the experimental groups, rats presented increased expression of acetylase (NAT1 and MEC-17) and decreased expression of deacetylase (Sirt2 and HDAC6) levels. Additionally, the expression of NAT1 and MEC-17 was gradually increased in DRG neurons following peripheral axonal injury compared to central axonal injury in a time-dependent manner. Conversely, the expression of Sirt2 and HDAC6 was gradually decreased in DRG neurons following peripheral axonal injury compared to central axonal injury in a time-dependent manner. CONCLUSIONS Our study indicated that insufficiency of acetylase and upregulation of deacetylase in DRG neurons after central axonal injury may contribute to the pathogenesis of cauda equine syndrome.
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