ABSTRACT
An intricate network of epigenetic factors regulates cell differentiation by modulating the chromatin structure and ultimately affecting gene expression. This review describes the chromatin landscape defining oligodendrocyte progenitor differentiation during development and remyelination. We shall discuss the current knowledge regarding modifications of chromatin components during the progression of progenitors into myelinating cells and discuss the potential contribution of histone variants, microRNAs, and DNA methylation. We shall also briefly address how changes to this chromatin landscape can disturb this natural progression and alter the capacity to remyelinate.
Subject(s)
Chromatin/genetics , Chromatin/pathology , Demyelinating Diseases/genetics , Demyelinating Diseases/pathology , Animals , Cell Differentiation/genetics , Demyelinating Diseases/metabolism , Epigenesis, Genetic/genetics , Humans , Multiple Sclerosis/genetics , Multiple Sclerosis/pathology , Stem Cells/metabolism , Stem Cells/pathologyABSTRACT
The process of oligodendrocyte differentiation is regulated by a dynamic interaction between a genetic and an epigenetic program. Recent studies, addressing nucleosomal histone modifications have considerably increased our knowledge regarding epigenetic regulation of gene expression during oligodendrocyte development and aging. These results have generated new hypotheses regarding the mechanisms underlying the decreased efficiency of endogenous remyelination in response to demyelinating injuries with increasing age. In this review, we present an overview of the epigenetic mechanisms regulating gene expression at specific stages of oligodendrocyte differentiation and maturation as well as the changes that occur with aging.