Roles of NG2‐glia in ischemic stroke

• Published in: CNS neuroscience & therapeutics Vol. 23; no. 7; pp. 547 - 553
• Main Authors: Song, Fei‐Er, Huang, Jia‐Lv, Lin, Si‐Han, Wang, Shuo, Ma, Guo‐Fen, Tong, Xiao‐Ping
• Format: Journal Article
• Language: English
• Published: England John Wiley & Sons, Inc 01.07.2017; John Wiley and Sons Inc
• Subjects: Animals; Brain injury; Brain Ischemia - drug therapy; Brain Ischemia - physiopathology; Central nervous system; Demyelinating diseases; Demyelination; Functional anatomy; Glial cells; Glial stem cells; Humans; Ion channels; Ischemia; Multiple sclerosis; Myelin; Neuromodulation; Neuronal-glial interactions; NG2‐glia; oligodendrocyte precursor cells; Oligodendrocyte Precursor Cells - drug effects; Oligodendrocyte Precursor Cells - physiology; Oligodendrocytes; Review; Stroke; Stroke - drug therapy; Stroke - physiopathology; oligodendrocyte precursor cells; NG2-glia; stroke; ischemia
• ISSN: 1755-5930; 1755-5949
• DOI: 10.1111/cns.12690

Summary Recent studies have shown that a widely distributed class of glial cells, termed NG2‐glia, engages in rapid signaling with surrounding neurons through direct synaptic contacts in the developing and mature central nervous system (CNS). This unique glial cell group has a typical function of proliferating and differentiating into oligodendrocytes during early development of the brain, which is crucial to axon myelin formation. Therefore, NG2‐glia are also called oligodendrocyte precursor cells (OPCs). In vitro and in vivo studies reveal that NG2‐glia expressing receptors and ion channels demonstrate functional significance for rapid signaling with neuronal synapses and modulation of neuronal activities in both physiological and pathological conditions. Although it is well known that NG2‐glia play an important role in demyelinating diseases such as multiple sclerosis, little is known about how NG2‐glia or OPCs impact neurons and brain function following ischemic injury. This review summarizes recent progress on the roles of NG2‐glia in ischemic stroke and illustrates new approaches for targeting NG2‐glia in the brain to treat this disease.