Logo image
Histone acetylation inhibitors promote axon growth in adult dorsal root ganglia neurons
Journal article   Open access   Peer reviewed

Histone acetylation inhibitors promote axon growth in adult dorsal root ganglia neurons

Shen Lin, Kutaiba Nazif, Alexander Smith, Peter W Baas and George M Smith
Journal of neuroscience research, v 93(8), pp 1215-1228
Aug 2015
PMID: 25702820
url
https://doi.org/10.1002/jnr.23573View
Published, Version of Record (VoR) Open

Abstract

Axons - enzymology Cells, Cultured Axons - drug effects Rats Rats, Sprague-Dawley Dose-Response Relationship, Drug Animals Ganglia, Spinal - enzymology Histone Acetyltransferases - antagonists & inhibitors Histone Acetyltransferases - metabolism Neurons - enzymology Anilides - pharmacology Histone Deacetylase Inhibitors - pharmacology Ganglia, Spinal - drug effects Neurons - drug effects Hydroxamic Acids - pharmacology
Intrinsic mechanisms that guide damaged axons to regenerate following spinal cord injury remain poorly understood. Manipulation of posttranslational modifications of key proteins in mature neurons could reinvigorate growth machinery after injury. One such modification is acetylation, a reversible process controlled by two enzyme families, the histone deacetylases (HDACs) and the histone acetyl transferases (HATs), acting in opposition. Whereas acetylated histones in the nucleus are associated with upregulation of growth-promoting genes, deacetylated tubulin in the axoplasm is associated with more labile microtubules, conducive to axon growth. This study investigates the effects of HAT and HDAC inhibitors on cultured adult dorsal root ganglia (DRG) neurons and shows that inhibition of HATs by anacardic acid or CPTH2 improves axon outgrowth, whereas inhibition of HDACs by TSA or tubacin inhibits axon growth. Anacardic acid increased the number of axons able to cross an inhibitory chondroitin sulfate proteoglycan border. Histone acetylation but not tubulin acetylation level was affected by HAT inhibitors, whereas tubulin acetylation levels were increased in the presence of the HDAC inhibitor tubacin. Although the microtubule-stabilizing drug taxol did not have an effect on the lengths of DRG axons, nocodazole decreased axon lengths. Determining the mechanistic basis will require future studies, but this study shows that inhibitors of HAT can augment axon growth in adult DRG neurons, with the potential of aiding axon growth over inhibitory substrates produced by the glial scar.

Metrics

13 Record Views
13 citations in Scopus

Details

UN Sustainable Development Goals (SDGs)

This publication has contributed to the advancement of the following goals:

#3 Good Health and Well-Being

InCites Highlights

Data related to this publication, from InCites Benchmarking & Analytics tool:

Collaboration types
Domestic collaboration
Web of Science research areas
Neurosciences
Logo image