Astrocyte roles in traumatic brain injury.
Astrocyte roles in traumatic brain injury.
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DOI：
10.1016/j.expneurol.2015.03.020
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发表时间：
2016-01
影响因子：
5.3
通讯作者：
Sofroniew MV
中科院分区：
文献类型：
--
作者：
Burda JE;Bernstein AM;Sofroniew MV
星形胶质细胞感知神经活动和细胞外空间组成的变化。作为响应，它们发挥对维持神经回路功能至关重要的稳态机制，例如缓冲神经递质、调节细胞外渗透压和校准神经血管耦合。除了维持正常的脑活动外，星形胶质细胞还对不同形式的脑损伤作出反应，其基因表达、形态、增殖能力和功能的异质性和进行性变化统称为反应性星形胶质细胞增生。创伤性脑损伤（TBI）引发复杂的事件，其中有害的机械力引起组织损伤并破坏中枢神经系统（CNS）稳态，这反过来触发随着时间的推移而演变的多种多细胞反应，并可导致神经修复或继发性细胞损伤。在对TBI的反应中，不同细胞微环境中的星形胶质细胞调节它们对不同程度的轴突损伤、血管破裂、缺血和炎症的反应性。在这里，我们审查不同形式的创伤性脑损伤诱导星形胶质细胞的反应和功能的后果，这些反应的创伤性脑损伤的病理生物学。关于星形胶质细胞对创伤后组织修复和突触重塑的贡献的证据进行了检查，并考虑了针对星形胶质细胞增生的特定方面以改善TBI后遗症的潜力。
Astrocytes sense changes in neural activity and extracellular space composition. In response, they exert homeostatic mechanisms critical for maintaining neural circuit function, such as buffering neurotransmitters, modulating extracellular osmolarity and calibrating neurovascular coupling. In addition to upholding normal brain activities, astrocytes respond to diverse forms of brain injury with heterogeneous and progressive changes of gene expression, morphology, proliferative capacity and function that are collectively referred to as reactive astrogliosis. Traumatic brain injury (TBI) sets in motion complex events in which noxious mechanical forces cause tissue damage and disrupt central nervous system (CNS) homeostasis, which in turn trigger diverse multi-cellular responses that evolve over time and can lead either to neural repair or secondary cellular injury. In response to TBI, astrocytes in different cellular microenvironments tune their reactivity to varying degrees of axonal injury, vascular disruption, ischemia and inflammation. Here we review different forms of TBI-induced astrocyte reactivity and the functional consequences of these responses for TBI pathobiology. Evidence regarding astrocyte contribution to post-traumatic tissue repair and synaptic remodeling is examined, and the potential for targeting specific aspects of astrogliosis to ameliorate TBI sequelae is considered.