Drebrin Upregulation Regulates Astrocyte Polarization and Supports Tissue Recovery After Spinal Cord Injury in Mice

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378041%3A_____%2F25%3A00636716" target="_blank" >RIV/68378041:_____/25:00636716 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216208:11130/25:10498670

Výsledek na webu

<a href="https://onlinelibrary.wiley.com/doi/10.1002/glia.70048" target="_blank" >https://onlinelibrary.wiley.com/doi/10.1002/glia.70048</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1002/glia.70048" target="_blank" >10.1002/glia.70048</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Drebrin Upregulation Regulates Astrocyte Polarization and Supports Tissue Recovery After Spinal Cord Injury in Mice

Popis výsledku v původním jazyce

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.

Název v anglickém jazyce

Drebrin Upregulation Regulates Astrocyte Polarization and Supports Tissue Recovery After Spinal Cord Injury in Mice

Popis výsledku anglicky

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.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30103 - Neurosciences (including psychophysiology)

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2025

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Glia

ISSN

0894-1491

e-ISSN

1098-1136

Svazek periodika

73

Číslo periodika v rámci svazku

9

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

15

Strana od-do

1910-1924

Kód UT WoS článku

001506794100001

EID výsledku v databázi Scopus

2-s2.0-105007743433