The K+–Cl↿/sup> Cotransporter KCC2 and Chloride Homeostasis: Potential Therapeutic Target in Acute Central Nervous System Injury
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  • 作者:Haijian Wu ; Xiaoru Che ; Junjia Tang ; Feiqiang Ma ; Kun Pan…
  • 关键词:KCC2 ; Chloride homeostasis ; Neuron ; Excitability ; Acute CNS injury
  • 刊名:Molecular Neurobiology
  • 出版年:2016
  • 出版时间:May 2016
  • 年:2016
  • 卷:53
  • 期:4
  • 页码:2141-2151
  • 全文大小:675 KB
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  • 作者单位:Haijian Wu (1)
    Xiaoru Che (3)
    Junjia Tang (1)
    Feiqiang Ma (2)
    Kun Pan (4)
    Mingfei Zhao (1)
    Anwen Shao (1)
    Qun Wu (1)
    Jianmin Zhang (1)
    Yuan Hong (1)

    1. Department of Neurosurgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, 88 Jiefang Road, Hangzhou, 310009, Zhejiang, China
    3. Department of Cardiology, Zhejiang Provincial People’s Hospital, Hangzhou, China
    2. Department of Emergency Medicine, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China
    4. Department of Neurosurgery, New York-Presbyterian Hospital, New York, NY, USA
  • 刊物主题:Neurosciences; Neurobiology; Cell Biology; Neurology;
  • 出版者:Springer US
  • ISSN:1559-1182
文摘
The K+–Cl− cotransporter-2 (KCC2) is a well-known member of the electroneutral cation-chloride cotransporters with a restricted expression pattern to neurons. This transmembrane protein mediates the efflux of Cl− out of neurons and exerts a critical role in inhibitory γ-aminobutyric acidergic (GABAergic) and glycinergic neurotransmission. Moreover, KCC2 participates in the regulation of various physiological processes of neurons, including cell migration, dendritic outgrowth, spine morphology, and dendritic synaptogenesis. It is important to note that down-regulation of KCC2 is associated with the pathogenesis of multiple neurological diseases, which is of particular relevance to acute central nervous system (CNS) injury. In this review, we aim to survey the pathogenic significance of KCC2 down-regulation under the condition of acute CNS injuries. We propose that further elucidation of the molecular mechanisms regarding KCC2 down-regulation after acute CNS injuries is necessary because of potential promising avenues for prevention and treatment of acute CNS injury.
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