Laser lesion in the mouse visual cortex induces a stem cell niche-like extracellular matrix, produced by immature astrocytes

  • The mammalian central nervous system (CNS) is characterized by a severely limited regeneration capacity. Comparison with lower species like amphibians, which are able to restore even complex tissues after damage, indicates the presence of an inhibitory environment that restricts the cellular response in mammals. In this context, signals provided by the extracellular matrix (ECM) are important regulators of events like cell survival, proliferation, migration, differentiation or neurite outgrowth. Therefore, knowledge of the post-lesional ECM and of cells that produce these factors might support development of new treatment strategies for patients suffering from traumatic brain injury and other types of CNS damage. In the present study, we analyzed the surround of focal infrared laser lesions of the adult mouse visual cortex. This lesion paradigm avoids direct contact with the brain, as the laser beam passes the intact bone. Cell type-specific markers revealed a distinct spatial distribution of different astroglial subtypes in the penumbra after injury. Glial fibrillary acidic protein (GFAP) as marker for reactive astrocytes was found broadly up-regulated, whereas the more immature markers vimentin and nestin were only expressed by a subset of cells. Dividing astrocytes could be identified via the proliferation marker Ki-67. Different ECM molecules, among others the neural stem cell-associated glycoprotein tenascin-C and the DSD-1 chondroitin sulfate epitope, were found on astrocytes in the penumbra. \(\textit {Wisteria floribunda}\) agglutinin (WFA) and aggrecan as markers for perineuronal nets, a specialized ECM limiting synaptic plasticity, appeared normal in the vicinity of the necrotic lesion core. In sum, expression of progenitor markers by astrocyte subpopulations and the identification of proliferating astrocytes in combination with an ECM that contains components typically associated with neural stem/progenitor cells suggest that an immature cell fate is facilitated as response to the injury.

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Metadaten
Author:Lars RollGND, Ulf EyselGND, Andreas FaissnerORCiDGND
URN:urn:nbn:de:hbz:294-73995
DOI:https://doi.org/10.3389/fncel.2020.00102
Parent Title (English):Frontiers in cellular neuroscience
Publisher:Frontiers Research Foundation
Place of publication:Lausanne
Document Type:Article
Language:English
Date of Publication (online):2020/08/10
Date of first Publication:2020/05/21
Publishing Institution:Ruhr-Universität Bochum, Universitätsbibliothek
Tag:Open Access Fonds
astrocyte; chondroitin sulfate; cortical plasticity; extracellular matrix; neural stem cell; niche; regeneration; tenascin
Volume:14
Issue:Article 102
First Page:102-1
Last Page:102-17
Note:
Article Processing Charge funded by the Deutsche Forschungsgemeinschaft (DFG) and the Open Access Publication Fund of Ruhr-Universität Bochum.
Institutes/Facilities:Lehrstuhl für Zellmorphologie und Molekulare Neurobiologie
Research Department of Neuroscience
Protein Research Department
open_access (DINI-Set):open_access
faculties:Fakultät für Biologie und Biotechnologie
International Graduate School of Neuroscience (IGSN)
Licence (English):License LogoCreative Commons - CC BY 4.0 - Attribution 4.0 International