Role of the lesion scar in the response to damage and repair of the central nervous system View Full Text


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Article Info

DATE

2012-02-25

AUTHORS

Hitoshi Kawano, Junko Kimura-Kuroda, Yukari Komuta, Nozomu Yoshioka, Hong Peng Li, Koki Kawamura, Ying Li, Geoffrey Raisman

ABSTRACT

Traumatic damage to the central nervous system (CNS) destroys the blood-brain barrier (BBB) and provokes the invasion of hematogenous cells into the neural tissue. Invading leukocytes, macrophages and lymphocytes secrete various cytokines that induce an inflammatory reaction in the injured CNS and result in local neural degeneration, formation of a cystic cavity and activation of glial cells around the lesion site. As a consequence of these processes, two types of scarring tissue are formed in the lesion site. One is a glial scar that consists in reactive astrocytes, reactive microglia and glial precursor cells. The other is a fibrotic scar formed by fibroblasts, which have invaded the lesion site from adjacent meningeal and perivascular cells. At the interface, the reactive astrocytes and the fibroblasts interact to form an organized tissue, the glia limitans. The astrocytic reaction has a protective role by reconstituting the BBB, preventing neuronal degeneration and limiting the spread of damage. While much attention has been paid to the inhibitory effects of the astrocytic component of the scars on axon regeneration, this review will cover a number of recent studies in which manipulations of the fibroblastic component of the scar by reagents, such as blockers of collagen synthesis have been found to be beneficial for axon regeneration. To what extent these changes in the fibroblasts act via subsequent downstream actions on the astrocytes remains for future investigation. More... »

PAGES

169-180

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1007/s00441-012-1336-5

    DOI

    http://dx.doi.org/10.1007/s00441-012-1336-5

    DIMENSIONS

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    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/22362507


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    35 schema:description Traumatic damage to the central nervous system (CNS) destroys the blood-brain barrier (BBB) and provokes the invasion of hematogenous cells into the neural tissue. Invading leukocytes, macrophages and lymphocytes secrete various cytokines that induce an inflammatory reaction in the injured CNS and result in local neural degeneration, formation of a cystic cavity and activation of glial cells around the lesion site. As a consequence of these processes, two types of scarring tissue are formed in the lesion site. One is a glial scar that consists in reactive astrocytes, reactive microglia and glial precursor cells. The other is a fibrotic scar formed by fibroblasts, which have invaded the lesion site from adjacent meningeal and perivascular cells. At the interface, the reactive astrocytes and the fibroblasts interact to form an organized tissue, the glia limitans. The astrocytic reaction has a protective role by reconstituting the BBB, preventing neuronal degeneration and limiting the spread of damage. While much attention has been paid to the inhibitory effects of the astrocytic component of the scars on axon regeneration, this review will cover a number of recent studies in which manipulations of the fibroblastic component of the scar by reagents, such as blockers of collagen synthesis have been found to be beneficial for axon regeneration. To what extent these changes in the fibroblasts act via subsequent downstream actions on the astrocytes remains for future investigation.
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    51 barriers
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    62 cytokines
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    66 effect
    67 extent
    68 fibroblastic component
    69 fibroblasts
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    71 formation
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    73 glia limitans
    74 glial cells
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    77 hematogenous cells
    78 inflammatory reaction
    79 inhibitory effect
    80 interface
    81 invasion
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    83 lesion scar
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