Journal Article

DZNE-2025-00922

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Drebrin Upregulation Regulates Astrocyte Polarization and Supports Tissue Recovery After Spinal Cord Injury in Mice.

Smejkalová, B. ; Ornaghi, M. ; Štěpánková, K. ; Schiweck, J.DZNE* ; Machová Urdzíková, L. ; Huelse, R. ; Mueller, S. ; Boehm-Sturm, P. ; Kwok, J. C. F. ; Fawcett, J. ; Murk, K. ; Eickholt, B. J. ; Jendelová, P.

2025
Wiley-Liss Bognor Regis [u.a.]

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Please use a persistent id in citations: doi:10.1002/glia.70048

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.

Keyword(s): Animals (MeSH) ; Spinal Cord Injuries: pathology (MeSH) ; Spinal Cord Injuries: metabolism (MeSH) ; Astrocytes: metabolism (MeSH) ; Astrocytes: pathology (MeSH) ; Neuropeptides: metabolism (MeSH) ; Neuropeptides: genetics (MeSH) ; Up-Regulation: physiology (MeSH) ; Recovery of Function: physiology (MeSH) ; Cell Polarity: physiology (MeSH) ; Cell Polarity: genetics (MeSH) ; Mice (MeSH) ; Mice, Knockout (MeSH) ; Mice, Inbred C57BL (MeSH) ; Disease Models, Animal (MeSH) ; Gliosis: pathology (MeSH) ; Gliosis: metabolism (MeSH) ; Female (MeSH) ; Spinal Cord: pathology (MeSH) ; Spinal Cord: metabolism (MeSH) ; immune cell infiltration ; neurodegeneration ; reactive astrogliosis ; spinal cord injury ; drebrins ; Neuropeptides

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Contributing Institute(s):

1. Axon Growth and Regeneration (AG Bradke)

Research Program(s):

1. 351 - Brain Function (POF4-351) (POF4-351)

Appears in the scientific report 2025

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Database coverage:
; ; ; BIOSIS Previews ; Biological Abstracts ; Clarivate Analytics Master Journal List ; Current Contents - Life Sciences ; DEAL Wiley ; Essential Science Indicators ; IF >= 5 ; JCR ; Nationallizenz ; SCOPUS ; Science Citation Index Expanded ; Web of Science Core Collection

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