Heterogeneity and Proliferative and Differential Regulators of NG2-glia in Physiological and Pathological States

Zuo      Zhang; Hongli      Zhou; Jiyin      Zhou
doi:10.2174/0929867326666190717112944
Abstract

NG2-glia, also called Oligodendrocyte Precursor Cells (OPCs), account for approximately 5%-10% of the cells in the developing and adult brain and constitute the fifth major cell population in the central nervous system. NG2-glia express receptors and ion channels involved in rapid modulation of neuronal activities and signaling with neuronal synapses, which have functional significance in both physiological and pathological states. NG2-glia participate in quick signaling with peripheral neurons via direct synaptic touches in the developing and mature central nervous system. These distinctive glia perform the unique function of proliferating and differentiating into oligodendrocytes in the early developing brain, which is critical for axon myelin formation. In response to injury, NG2-glia can proliferate, migrate to the lesions, and differentiate into oligodendrocytes to form new myelin sheaths, which wrap around damaged axons and result in functional recovery. The capacity of NG2-glia to regulate their behavior and dynamics in response to neuronal activity and disease indicate their critical role in myelin preservation and remodeling in the physiological state and in repair in the pathological state. In this review, we provide a detailed summary of the characteristics of NG2-glia, including their heterogeneity, the regulators of their proliferation, and the modulators of their differentiation into oligodendrocytes.
Keywords: NG2-glia, oligodendrocyte precursor cells, heterogeneity, differentiation, oligodendrocyte, myelin sheaths.
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DOI https://dx.doi.org/10.2174/0929867326666190717112944	Print ISSN 0929-8673
Publisher Name Bentham Science Publisher	Online ISSN 1875-533X
Current Medicinal Chemistry

Heterogeneity and Proliferative and Differential Regulators of NG2-glia in Physiological and Pathological States

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