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INVITED REVIEW
Year : 2017  |  Volume : 12  |  Issue : 12  |  Page : 1964-1970

Environmental cues determine the fate of astrocytes after spinal cord injury


Shriners Hospitals Pediatric Research Center, Department of Anatomy and Cell Biology, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, USA

Correspondence Address:
Shuxin Li
Shriners Hospitals Pediatric Research Center, Department of Anatomy and Cell Biology, Lewis Katz School of Medicine at Temple University, Philadelphia, PA
USA
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Source of Support: This work was supported by research grants to SL from NIH (1R01NS079432 and 1R01EY024575) and Shriners Research Foundation (SHC-86300-PHI, SHC-86200-PHI-16 and SHC-85100)., Conflict of Interest: None


DOI: 10.4103/1673-5374.221144

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Reactive astrogliosis occurs after central nervous system (CNS) injuries whereby resident astrocytes form rapid responses along a graded continuum. Following CNS lesions, naïve astrocytes are converted into reactive astrocytes and eventually into scar-forming astrocytes that block axon regeneration and neural repair. It has been known for decades that scarring development and its related extracellular matrix molecules interfere with regeneration of injured axons after CNS injury, but the cellular and molecular mechanisms for controlling astrocytic scar formation and maintenance are not well known. Recent use of various genetic tools has made tremendous progress in better understanding genesis of reactive astrogliosis. Especially, the latest experiments demonstrate environment-dependent plasticity of reactive astrogliosis because reactive astrocytes isolated from injured spinal cord form scarring astrocytes when transplanted into injured spinal cord, but revert in retrograde to naive astrocytes when transplanted into naive spinal cord. The interactions between upregulated type I collagen and its receptor integrin β1 and the N-cadherin-mediated cell adhesion appear to play major roles for local astrogliosis around the lesion. This review centers on the environment-dependent plasticity of reactive astrogliosis after spinal cord injury and its potential as a therapeutic target.


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