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Histone deacetylase inhibitors preserve function in aging axons
Author(s) -
Baltan Selva
Publication year - 2012
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2012.07949.x
Subject(s) - histone deacetylase , hdac11 , hdac10 , histone deacetylase 5 , neuroscience , histone deacetylase 2 , function (biology) , histone , microbiology and biotechnology , chemistry , biology , biochemistry , dna
Aging increases the vulnerability of aging white matter to ischemic injury. Histone deacetylase ( HDAC ) inhibitors preserve young adult white matter structure and function during ischemia by conserving ATP and reducing excitotoxicity. In isolated optic nerve from 12‐month‐old mice, deprived of oxygen and glucose, we show that pan‐ and Class I‐specific HDAC inhibitors promote functional recovery of axons. This protection correlates with preservation of axonal mitochondria. The cellular expression of HDAC 3 in the central nervous system ( CNS ), and HDAC 2 in optic nerve considerably changed with age, expanding to more cytoplasmic domains from nuclear compartments, suggesting that changes in glial cell protein acetylation may confer protection to aging axons. Our results indicate that manipulation of HDAC activities in glial cells may have a universal potential for stroke therapy across age groups.