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Drebrin controls scar formation and astrocyte reactivity upon traumatic brain injury by regulating membrane trafficking

Author

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  • Juliane Schiweck

    (Charité - Universitätsmedizin Berlin)

  • Kai Murk

    (Charité - Universitätsmedizin Berlin)

  • Julia Ledderose

    (Charité - Universitätsmedizin Berlin)

  • Agnieszka Münster-Wandowski

    (Charité - Universitätsmedizin Berlin)

  • Marta Ornaghi

    (Charité - Universitätsmedizin Berlin)

  • Imre Vida

    (Charité - Universitätsmedizin Berlin)

  • Britta J. Eickholt

    (Charité - Universitätsmedizin Berlin
    Charité - Universitätsmedizin Berlin)

Abstract

The brain of mammals lacks a significant ability to regenerate neurons and is thus particularly vulnerable. To protect the brain from injury and disease, damage control by astrocytes through astrogliosis and scar formation is vital. Here, we show that brain injury in mice triggers an immediate upregulation of the actin-binding protein Drebrin (DBN) in astrocytes, which is essential for scar formation and maintenance of astrocyte reactivity. In turn, DBN loss leads to defective astrocyte scar formation and excessive neurodegeneration following brain injuries. At the cellular level, we show that DBN switches actin homeostasis from ARP2/3-dependent arrays to microtubule-compatible scaffolds, facilitating the formation of RAB8-positive membrane tubules. This injury-specific RAB8 membrane compartment serves as hub for the trafficking of surface proteins involved in astrogliosis and adhesion mediators, such as β1-integrin. Our work shows that DBN-mediated membrane trafficking in astrocytes is an important neuroprotective mechanism following traumatic brain injury in mice.

Suggested Citation

  • Juliane Schiweck & Kai Murk & Julia Ledderose & Agnieszka Münster-Wandowski & Marta Ornaghi & Imre Vida & Britta J. Eickholt, 2021. "Drebrin controls scar formation and astrocyte reactivity upon traumatic brain injury by regulating membrane trafficking," Nature Communications, Nature, vol. 12(1), pages 1-16, December.
    • Handle: RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-21662-x
    DOI: 10.1038/s41467-021-21662-x
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    Cited by:

    1. T. M. O’Shea & Y. Ao & S. Wang & A. L. Wollenberg & J. H. Kim & R. A. Ramos Espinoza & A. Czechanski & L. G. Reinholdt & T. J. Deming & M. V. Sofroniew, 2022. "Lesion environments direct transplanted neural progenitors towards a wound repair astroglial phenotype in mice," Nature Communications, Nature, vol. 13(1), pages 1-22, December.

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