In the presence of danger:the extracellular matrix defensive response to central nervous system injury
Lyn B. Jakeman
Kent E. Williams
Bryan Brautigam
摘要：Glial cells in the central nervous system (CNS) contribute to formation of the extracellular matrix, which provides adhesive sites, signaling molecules, and a diffusion barrier to enhance efifcient neurotransmission and axon potential propagation. In the normal adult CNS, the extracellular matrix (ECM) is relatively stable except in selected regions characterized by dynamic remodel-ing. However, after trauma such as a spinal cord injury or cortical contusion, the lesion epicenter becomes a focus of acute neuroinlfammation. The activation of the surrounding glial cells leads to a dramatic change in the composition of the ECM at the edges of the lesion, creating a perile-sion environment dominated by growth inhibitory molecules and restoration of the peripheral/central nervous system border. An advantage of this response is to limit the invasion of damaging cells and diffusion of toxic molecules into the spared tissue regions, but this occurs at the cost of inhibiting migration of endogenous repair cells and preventing axonal regrowth. The following review was prepared by reading and discussing over 200 research articles in the ifeld published in PubMed and selecting those with signiifcant impact and/or controversial points. This article highlights structural and functional features of the normal adult CNS ECM and then focuses on the reactions of glial cells and changes in the perilesion border that occur following spinal cord or contusive brain injury. Current research strategies directed at modifying the inhibitory perile-sion microenvironment without eliminating the protective functions of glial cell activation are discussed.
机标关键词：central nervous systemextracellular matrixspinal cord injurydiffusion barrierbrain injuryglial cell
资助基金：The study was supported by NIH/NINDS R01-NS043246, P30-NS045758, the Interna-tional Spinal Research Trust(STR-100)
论文发表日期：2014-01-01
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：8( 377-384 )
英文信息