Abstract
Like other CNS neurons, mature retinal ganglion cells (RGCs) cannot regenerate their axons after nerve injury due to loss of regenerative capacity. One of the reasons why they lose their capacity seems to be a dramatic shift in gene expression of RGCs under epigenetic modulation. In here, we found that levels of histone H3 lysine 9 acetylation decreased after birth in RGCs. This decrease showed good correlation with restriction of retinoic acid receptor β (RARβ) expression in RGCs after birth. Furthermore, we demonstrated that a histone deacetylase inhibitor, trichostatin A, induced axonal regeneration of adult rat RGCs through RARβ induction.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Acetylation / drug effects
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Animals
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Axons / physiology*
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Cells, Cultured
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Gene Expression / drug effects*
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Histone Deacetylase Inhibitors / pharmacology*
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Histones / metabolism*
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Hydroxamic Acids / pharmacology*
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Male
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Nerve Regeneration / drug effects*
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Nerve Regeneration / genetics*
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Neurogenesis / drug effects*
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Neurogenesis / genetics*
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Rats
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Rats, Sprague-Dawley
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Receptors, Retinoic Acid / genetics*
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Receptors, Retinoic Acid / metabolism*
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Retinal Ganglion Cells / metabolism
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Retinal Ganglion Cells / physiology*
Substances
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Histone Deacetylase Inhibitors
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Histones
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Hydroxamic Acids
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Receptors, Retinoic Acid
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retinoic acid receptor beta
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trichostatin A