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Published on: May 31, 2017
Class II HDACs and neuronal regeneration.
1Department of Biochemistry, Yong Loo Lin School of Medicine, National University Health System, Singapore, Singapore; NUS Graduate School for Integrative Sciences and Engineering, National University of Singapore, Medical Drive, Singapore, 117597, Singapore.
Peripheral nerve axons regenerate better than central nervous system (CNS) axons partly due to growth cone formation. Histone deacetylase (HDAC) inhibitors show promise for enhancing axonal regeneration by modulating neuronal processes.
Area of Science:
- Neuroscience
- Molecular Biology
- Regenerative Medicine
Background:
- Peripheral nerve axons exhibit superior regenerative capacity compared to central nervous system (CNS) neurons.
- Growth cone formation is crucial for axonal regeneration and involves microtubule organization.
- Histone deacetylases (HDACs) regulate critical neuronal functions, including differentiation, survival, and degeneration.
Purpose of the Study:
- To explore the role of HDACs in axonal regeneration.
- To discuss how manipulating HDAC activity, especially Type II HDACs, can enhance nerve repair.
Main Methods:
- Review of recent advances in HDAC research related to neuronal regeneration.
- Focus on the deacetylase activity of HDAC5 and HDAC6 on tubulin.
Main Results:
- HDAC inhibitors have demonstrated efficacy in reducing neuronal death and promoting neurite outgrowth.
- Specific HDACs, like HDAC5 and HDAC6, deacetylate tubulin, a key component of microtubules.
Conclusions:
- Targeting HDAC activity, particularly HDAC5 and HDAC6, presents a promising therapeutic strategy for promoting axonal regeneration in the nervous system.
- Understanding the mechanisms of HDACs in tubulin deacetylation can lead to novel treatments for nerve injury.
