Oligodendrocytes Development and Wnt Signaling Pathway - Oligodendrocytes Development and Wnt Signaling Pathway - Open Access Pub

Oligodendrocytes are specialized glial cell in central nervous system (CNS) responsible for the formation of myelin sheath around the axon. Oligodendrocyte proliferation and differentiation is regulated by Wnt signaling pathway, at various stages. However, different study groups have described controversial conclusions about the effect of Wnt on oligodendrocytes precursor cells (OPCs) development. Initially it has been proposed that Wnt pathway negatively regulates the OPCs proliferation and differentiation but recently some studies have described that Wnt promotes the differentiation of OPCs. After carefully reviewing the literature, we believe that Wnt play multiple roles in OPCs differentiation and its function is time (stage) and dose sensitive. Low to moderate activation of Wnt promotes OPC development, while too much or too low is inhibitory. Current evidences also suggested that in early developmental stages, Wnt inhibits the OPCs formation from neural progenitors and differentiation into immature oligodendrocytes. But in late stages Wnt plays promoting role in differentiation and maturation of oligodendrocytes. This review summarized the updated information regarding the critical role of Wnt signaling cascade in proliferation and differentiation of OPCs. DOI10.14302/issn.2577-2279.ijha-18-2407 Oligodendrocytes (OLs) are specialized glial cell in central nervous system (CNS) responsible for the formation of myelin sheath around the axon which not only help in rapid conduction of electrical impulses but also provides metabolic and trophic support to underlying axon. Loss or damage to myelin sheath may result in various devastating neurological disorders including multiple sclerosis (MS), cerebral palsy and others 1, 2, 3, 4. Fortunately, the CNS has an excellent capacity to regenerate myelin sheath, in healthy individuals as well as in the early course of diseases 5. However, during a prolonged disease course with recurrent attacks of demyelination, remyelination eventually fails leading to various demyelinating diseases 6, 7, 8. It is therefore critical to understand the cellular and molecular mechanisms that regulate myelination in order to develop novel therapies to target remyelination 2, 9, 10, 11, 12, 13. In mammals, myelination process occurs during postnatal development 14, 15. OLs development, from an oligodendrocyte precursor cell (OPC) to a mature myelinating OL, is controlled by a number of both inhibitory and inductive factors. Either failure of the mechanisms that promote myelination or the presences of strong inhibitory molecular