Authors
Leo Shimizu, Ryo Asahina, Toshio Ohshima
Published in
Molecular and cellular neurosciences. Pages 104129. Oct 19, 2026. Epub Oct 19, 2026.
Abstract
Reactive astrocytes play a central role in shaping the post-injury microenvironment after spinal cord injury (SCI), yet the molecular mechanisms governing their proliferative expansion and contribution to scar architecture remain incompletely defined. Conditional deletion of CRMP4 in astrocytes significantly reduced astrocyte proliferation, altered scar organization, and attenuated the inflammatory milieu surrounding the lesion, including reduced microglial activation. These changes were accompanied by significantly improved locomotor recovery, as assessed by the Basso Mouse Scale (BMS) locomotor rating scale, indicating enhanced functional restoration after SCI. Our findings suggest that CRMP4 promotes the expansion of reactive astrocyte subsets that shape the inhibitory niche surrounding the lesion core, thereby restricting axonal regeneration and limiting functional recovery after SCI. Single-cell RNA sequencing (scRNA-seq) analysis of a public dataset revealed that Crmp4 expression is enriched in proliferative, progenitor-like astrocyte subpopulations that contribute to scar formation, including subclusters corresponding to the G2/M phases of the cell cycle. Together, this study identifies astrocytic CRMP4 as a key molecular determinant of reactive astrocyte dynamics and scar architecture after SCI, providing new insight into cell-type-specific regulation of glial responses in central nervous system injury.
PMID:
42896692
Bibliographic data and abstract were imported from PubMed on 20 Oct 2026.
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