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@ARTICLE{Smejkalov:280244,
author = {Smejkalová, Barbora and Ornaghi, Marta and Štěpánková,
Kateřina and Schiweck, Juliane and Machová Urdzíková,
Lucia and Huelse, Robert and Mueller, Susanne and
Boehm-Sturm, Philipp and Kwok, Jessica C F and Fawcett,
James and Murk, Kai and Eickholt, Britta J and Jendelová,
Pavla},
title = {{D}rebrin {U}pregulation {R}egulates {A}strocyte
{P}olarization and {S}upports {T}issue {R}ecovery {A}fter
{S}pinal {C}ord {I}njury in {M}ice.},
journal = {Glia},
volume = {73},
number = {9},
issn = {0894-1491},
address = {Bognor Regis [u.a.]},
publisher = {Wiley-Liss},
reportid = {DZNE-2025-00922},
pages = {1910 - 1924},
year = {2025},
abstract = {Spinal cord injury (SCI) results in significant disruption
of nerve fibers responsible for transmitting signals between
the brain and body, often leading to partial or complete
motor, sensory, and autonomic dysfunction below the injury
site. Astrocytes are an important component in scar
formation, crucial for suppression of injury propagation,
effective wound healing, and the regulation of neuronal
plasticity. Here, we identify the role of the actin-binding
protein Drebrin (DBN) in reactive astrogliosis following
SCI. SCI induces the upregulation of DBN in astrocytes,
which controls immediate injury containment but also the
long-term preservation of tissue integrity and healing in
the spinal cord. DBN knockout results in enlarged spinal
cord lesions, increased immune cell infiltration, and
neurodegeneration. Mechanistically, DBN loss disrupts the
polarization of scar border-forming astrocytes, leading to
impaired encapsulation of the injury. In summary, DBN serves
as a pivotal regulator of SCI outcome by modulating
astrocytic polarity, which is essential for establishing a
protective barrier confining the lesion site.},
keywords = {Animals / Spinal Cord Injuries: pathology / Spinal Cord
Injuries: metabolism / Astrocytes: metabolism / Astrocytes:
pathology / Neuropeptides: metabolism / Neuropeptides:
genetics / Up-Regulation: physiology / Recovery of Function:
physiology / Cell Polarity: physiology / Cell Polarity:
genetics / Mice / Mice, Knockout / Mice, Inbred C57BL /
Disease Models, Animal / Gliosis: pathology / Gliosis:
metabolism / Female / Spinal Cord: pathology / Spinal Cord:
metabolism / immune cell infiltration (Other) /
neurodegeneration (Other) / reactive astrogliosis (Other) /
spinal cord injury (Other) / drebrins (NLM Chemicals) /
Neuropeptides (NLM Chemicals)},
cin = {AG Bradke},
ddc = {610},
cid = {I:(DE-2719)1013002},
pnm = {351 - Brain Function (POF4-351)},
pid = {G:(DE-HGF)POF4-351},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:40497424},
pmc = {pmc:PMC12313004},
doi = {10.1002/glia.70048},
url = {https://pub.dzne.de/record/280244},
}