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Lange Canhos, L. ; Chen, M.* ; Falk, S. ; Popper, B.* ; Straub, T.* ; Götz, M. ; Sirko, S.

Repetitive injury and absence of monocytes promote astrocyte self-renewal and neurological recovery.

Glia 69, 165-181 (2021)
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Open Access Gold (Paid Option)
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Unlike microglia and NG2 glia, astrocytes are incapable of migrating to sites of injury in the posttraumatic cerebral cortex, instead relying on proliferation to replenish their numbers and distribution in the affected region. However, neither the spectrum of their proliferative repertoire nor their postinjury distribution has been examined in vivo. Using a combination of different thymidine analogs and clonal analysis in a model of repetitive traumatic brain injury, we show for the first time that astrocytes that are quiescent following an initial injury can be coerced to proliferate after a repeated insult in the cerebral cortex grey matter. Interestingly, this process is promoted by invasion of monocytes to the injury site, as their genetic ablation (using CCR2(-/-)mice) increased the number of repetitively dividing astrocytes at the expense of newly proliferating astrocytes in repeatedly injured parenchyma. These differences profoundly affected both the distribution of astrocytes and recovery period for posttraumatic behavior deficits suggesting key roles of astrocyte self-renewal in brain repair after injury.
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Publication type Article: Journal article
Document type Scientific Article
Keywords Astrocyte Topology ; Cognitive Disfunction ; Inflammation ; Reactive Gliosis ; Self-renew ; Tbi; Experimental Autoimmune Encephalomyelitis; Traumatic Brain-injury; Focal Laser-lesions; Extracellular-matrix; Reactive Astrocytes; Cerebral-cortex; Neural Stem; Cortical Plasticity; Clonal Expansion; Cells
ISSN (print) / ISBN 0894-1491
e-ISSN 1098-1136
Journal Glia
Quellenangaben Volume: 69, Issue: 1, Pages: 165-181 Article Number: , Supplement: ,
Publisher Wiley
Publishing Place 111 River St, Hoboken 07030-5774, Nj Usa
Reviewing status Peer reviewed