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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},
}