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Environmental Cues Determine the Fate of Astrocytes After Spinal Cord Injury

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Date 2018 Jan 12
PMID 29323029
Citations 16
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Abstract

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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References
1.
Lengyel E, Wang H, Stepp E, Juarez J, Wang Y, Doe W . Requirement of an upstream AP-1 motif for the constitutive and phorbol ester-inducible expression of the urokinase-type plasminogen activator receptor gene. J Biol Chem. 1996; 271(38):23176-84. DOI: 10.1074/jbc.271.38.23176. View

2.
Kumamaru H, Ohkawa Y, Saiwai H, Yamada H, Kubota K, Kobayakawa K . Direct isolation and RNA-seq reveal environment-dependent properties of engrafted neural stem/progenitor cells. Nat Commun. 2012; 3:1140. DOI: 10.1038/ncomms2132. View

3.
Barnabe-Heider F, Goritz C, Sabelstrom H, Takebayashi H, Pfrieger F, Meletis K . Origin of new glial cells in intact and injured adult spinal cord. Cell Stem Cell. 2010; 7(4):470-82. DOI: 10.1016/j.stem.2010.07.014. View

4.
Gris P, Tighe A, Levin D, Sharma R, Brown A . Transcriptional regulation of scar gene expression in primary astrocytes. Glia. 2007; 55(11):1145-55. DOI: 10.1002/glia.20537. View

5.
Seifert G, Schilling K, Steinhauser C . Astrocyte dysfunction in neurological disorders: a molecular perspective. Nat Rev Neurosci. 2006; 7(3):194-206. DOI: 10.1038/nrn1870. View