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

Juliane Schiweck, Kai Murk (), Julia Ledderose, Agnieszka Münster-Wandowski, Marta Ornaghi, Imre Vida and Britta J. Eickholt ()
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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

Nature Communications, 2021, vol. 12, issue 1, 1-16

Abstract: 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.

Date: 2021
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DOI: 10.1038/s41467-021-21662-x

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