title: Unwrapping Neurotrophic Cytokines and Histone Modification.
abstract: The conventional view that neuroinflammatory lesions contain strictly pro- and anti-inflammatory cytokines is being challenged. Some proinflammatory products e.g. TNF-α are crucial intermediates in axon regeneration, oligodendroglial renewal and remyelination. A more functional system of nomenclature classifies cytokines by their neuro 'protective' or 'suppressive' properties. Beyond the balance of these 'environmental' or 'extrinsic' signals, specific 'intrinsic' determinants of cytokine signalling appear to influence the outcome of axoglial regeneration. In this commentary, we examine the potential importance of cytokine-induced histone modification on oligodendrocyte differentiation. Neuroinflammation mediates the release of astrocytic leukaemia inhibitory factor (LIF) and erythropoietin (EPO) which potentiates oligodendrocyte differentiation and myelin production. Meanwhile, histone deacetylation strongly suppresses important inhibitors of oligodendrocyte differentiation. Given that LIF and EPO induce histone deacetylases in other systems, future studies should examine whether this mechanism significantly influences the outcome of cytokine-induced remyelination, and whether epigenetic drug targets could potentiate the effects of exogenous cytokine therapy.
authors.affiliation: Brighton and Sussex Medical School, The Audrey Emerton Building, Eastern Road, Kemp Town, Brighton, BN2 5BE, UK. c.roe1@uni.bsms.ac.uk.
authors.forename: Cieron
authors.initials: C
authors.lastname: Roe
mesh_terms: D000818:Animals; D002462:Cell Membrane / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism*; D042421:Histone Code / Q000502:physiology; D006655:Histone Deacetylases / Q000378:metabolism*; D006657:Histones / Q000378:metabolism*; D006801:Humans; D009414:Nerve Growth Factors / Q000378:metabolism*
chemical_list: D016207:Cytokines; D006657:Histones; D009414:Nerve Growth Factors; D006655:Histone Deacetylases
keywords: Epigenetics; Histone modification; Myelination; Neurodegeneration; Neurotrophic cytokines; Oligodendrocytes; Therapy