Differential Expression of Tubulin Acetylase and Deacetylase Between the Damaged Central and Peripheral Branch of Dorsal Root Ganglion Neurons.
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.
Publication Date: 2017-07-28 PubMed ID: 28753589PubMed Central: PMC5545626DOI: 10.12659/msm.902829Google Scholar: Lookup
The Equine Research Bank provides access to a large database of publicly available scientific literature. Inclusion in the Research Bank does not imply endorsement of study methods or findings by Mad Barn.
- Journal Article
Summary
This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.
This research investigates the differences between the peripheral and central branches of the dorsal root ganglion (DRG) in rats, with a focus on the expression of acetylase and deacetylase in relation to axonal injury.
Research Background
- The study seeks to gain a deeper understanding of the differences between the peripheral and central branches of the DRG neurons. DRG neurons are responsible for transmitting information from peripheral sensory receptors to the spinal cord, with each neuron having a peripheral and central branch.
- In particular, the research focuses on the role of tubulin post-translational modifications, such as acetylation and deacetylation, in these neurons after damage. This process is involved in the regulation of neuronal plasticity and function.
- The insufficiency of acetylase and upregulation of deacetylase in DRG neurons after central axonal injury has been proposed as a potential contributing factor to the pathogenesis of cauda equine syndrome.
Methodology
- The experiment involved fifty Sprague-Dawley rats, that were divided into five groups. Different injuries were inflicted upon the rats – spinal nerve ligation (SNL) and cauda equina compression (CEC), at different times, alongside a control group.
- The research team analyzed the expression profile of acetylase and deacetylase within the DRG neurons, using real-time PCR, Western blotting, and immunohistochemistry techniques.
Findings
- The results demonstrated increased expression of acetylase and decreased expression of deacetylase in the DRG neurons of the rats that were subjected to peripheral axonal injuries.
- The expression levels of acetylase increased over time following peripheral axonal injury, while the expression of deacetylase decreased over time.
- On the other hand, central axonal injury did not follow the same pattern of expression, pointing to differential responses within the DRG neurons based on the type of injury.
Conclusion
- The research concluded that acetylase and deacetylase play different roles in the peripheral and central branches of the DRG neurons after axonal injury.
- These findings shed light on the pathogenesis of cauda equine syndrome, with the insufficiency of acetylase and upregulation of deacetylase in DRG neurons potentially contributing to this condition following central axonal injury.
Cite This Article
APA
Fu Z, Shi J.
(2017).
Differential Expression of Tubulin Acetylase and Deacetylase Between the Damaged Central and Peripheral Branch of Dorsal Root Ganglion Neurons.
Med Sci Monit, 23, 3673-3678.
https://doi.org/10.12659/msm.902829 Publication
Researcher Affiliations
- Department of Orthopedics, Changzheng Hospital, Second Military Medical University of China, Shanghai, China (mainland).
- Department of Orthopedics, Changzheng Hospital, Second Military Medical University of China, Shanghai, China (mainland).
MeSH Terms
- Acetylation
- Animals
- Ganglia, Spinal / metabolism
- Ganglia, Spinal / physiology
- Hyperalgesia / etiology
- Neurons / metabolism
- Peripheral Nervous System Diseases
- Polyradiculopathy / metabolism
- Protein Processing, Post-Translational
- Rats
- Rats, Sprague-Dawley
- Spinal Nerves / metabolism
- Transcriptome
- Tubulin / metabolism
- Tubulin Modulators / metabolism
References
This article includes 23 references
- Ma B, Wu H, Jia LS, Yuan W, Shi GD, Shi JG. Cauda equina syndrome: a review of clinical progress.. Chin Med J (Engl) 2009 May 20;122(10):1214-22.
- Huebner EA, Strittmatter SM. Axon regeneration in the peripheral and central nervous systems.. Results Probl Cell Differ 2009;48:339-51.
- Neumann S, Skinner K, Basbaum AI. Sustaining intrinsic growth capacity of adult neurons promotes spinal cord regeneration.. Proc Natl Acad Sci U S A 2005 Nov 15;102(46):16848-52.
- Akhmanova A, Steinmetz MO. Tracking the ends: a dynamic protein network controls the fate of microtubule tips.. Nat Rev Mol Cell Biol 2008 Apr;9(4):309-22.
- Janke C, Kneussel M. Tubulin post-translational modifications: encoding functions on the neuronal microtubule cytoskeleton.. Trends Neurosci 2010 Aug;33(8):362-72.
- Matus A. Microtubule-associated proteins: their potential role in determining neuronal morphology.. Annu Rev Neurosci 1988;11:29-44.
- Westermann S, Weber K. Post-translational modifications regulate microtubule function.. Nat Rev Mol Cell Biol 2003 Dec;4(12):938-47.
- Sirajuddin M, Rice LM, Vale RD. Regulation of microtubule motors by tubulin isotypes and post-translational modifications.. Nat Cell Biol 2014 Apr;16(4):335-44.
- Liu X, Fu Z, Wu Y, Hu X Jr, Zhu T Jr, Jin C Jr. Neuroprotective effect of hydrogen sulfide on acute cauda equina injury in rats.. Spine J 2016 Mar;16(3):402-7.
- Shi J, Jia L, Yuan W, Shi G, Ma B, Wang B, Wu J. Clinical classification of cauda equina syndrome for proper treatment.. Acta Orthop 2010 Jun;81(3):391-5.
- Conde C, Cáceres A. Microtubule assembly, organization and dynamics in axons and dendrites.. Nat Rev Neurosci 2009 May;10(5):319-32.
- Poulain FE, Sobel A. The microtubule network and neuronal morphogenesis: Dynamic and coordinated orchestration through multiple players.. Mol Cell Neurosci 2010 Jan;43(1):15-32.
- Garnham CP, Roll-Mecak A. The chemical complexity of cellular microtubules: tubulin post-translational modification enzymes and their roles in tuning microtubule functions.. Cytoskeleton (Hoboken) 2012 Jul;69(7):442-63.
- Janke C, Bulinski JC. Post-translational regulation of the microtubule cytoskeleton: mechanisms and functions.. Nat Rev Mol Cell Biol 2011 Nov 16;12(12):773-86.
- Hellal F, Hurtado A, Ruschel J, Flynn KC, Laskowski CJ, Umlauf M, Kapitein LC, Strikis D, Lemmon V, Bixby J, Hoogenraad CC, Bradke F. Microtubule stabilization reduces scarring and causes axon regeneration after spinal cord injury.. Science 2011 Feb 18;331(6019):928-31.
- Sengottuvel V, Leibinger M, Pfreimer M, Andreadaki A, Fischer D. Taxol facilitates axon regeneration in the mature CNS.. J Neurosci 2011 Feb 16;31(7):2688-99.
- Wloga D, Gaertig J. Post-translational modifications of microtubules.. J Cell Sci 2010 Oct 15;123(Pt 20):3447-55.
- Dompierre JP, Godin JD, Charrin BC, Cordelières FP, King SJ, Humbert S, Saudou F. Histone deacetylase 6 inhibition compensates for the transport deficit in Huntington's disease by increasing tubulin acetylation.. J Neurosci 2007 Mar 28;27(13):3571-83.
- Reed NA, Cai D, Blasius TL, Jih GT, Meyhofer E, Gaertig J, Verhey KJ. Microtubule acetylation promotes kinesin-1 binding and transport.. Curr Biol 2006 Nov 7;16(21):2166-72.
- d'Ydewalle C, Krishnan J, Chiheb DM, Van Damme P, Irobi J, Kozikowski AP, Vanden Berghe P, Timmerman V, Robberecht W, Van Den Bosch L. HDAC6 inhibitors reverse axonal loss in a mouse model of mutant HSPB1-induced Charcot-Marie-Tooth disease.. Nat Med 2011 Jul 24;17(8):968-74.
- Li L, Wei D, Wang Q, Pan J, Liu R, Zhang X, Bao L. MEC-17 deficiency leads to reduced α-tubulin acetylation and impaired migration of cortical neurons.. J Neurosci 2012 Sep 12;32(37):12673-83.
- Kalebic N, Sorrentino S, Perlas E, Bolasco G, Martinez C, Heppenstall PA. αTAT1 is the major α-tubulin acetyltransferase in mice.. Nat Commun 2013;4:1962.
- Aguilar A, Becker L, Tedeschi T, Heller S, Iomini C, Nachury MV. Α-tubulin K40 acetylation is required for contact inhibition of proliferation and cell-substrate adhesion.. Mol Biol Cell 2014 Jun 15;25(12):1854-66.
Citations
This article has been cited 2 times.- Zhao Q, Jiang C, Zhao L, Dai X, Yi S. Unleashing Axonal Regeneration Capacities: Neuronal and Non-neuronal Changes After Injuries to Dorsal Root Ganglion Neuron Central and Peripheral Axonal Branches.. Mol Neurobiol 2023 Aug 24;.
- Zhang Y, Chi D. Overexpression of SIRT2 Alleviates Neuropathic Pain and Neuroinflammation Through Deacetylation of Transcription Factor Nuclear Factor-Kappa B.. Inflammation 2018 Mar;41(2):569-578.
Use Nutrition Calculator
Check if your horse's diet meets their nutrition requirements with our easy-to-use tool Check your horse's diet with our easy-to-use tool
Talk to a Nutritionist
Discuss your horse's feeding plan with our experts over a free phone consultation Discuss your horse's diet over a phone consultation
Submit Diet Evaluation
Get a customized feeding plan for your horse formulated by our equine nutritionists Get a custom feeding plan formulated by our nutritionists
