ArticleFrontiers in neural circuits2026
Loss of function of Noggin inhibits glial scar formation and motor function recovery after spinal cord injury.
Article in Frontiers in neural circuits, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Noggin is a glycosylated protein that acts as an antagonist of bone morphogenetic proteins and has been implicated in astrogliosis and functional recovery after spinal cord injury (SCI). Although Noggin is known to regulate astrocytic responses, its role in reactive astrogliosis and glial scar formation after SCI remains unclear. Under normal conditions, Noggin is expressed in astrocytes in the white matter of the mouse spinal cord. In this study, we investigated the role of Noggin in reactive astrogliosis and glial scar formation after SCI. Methods: We first examined the expression pattern of Noggin in the mouse spinal cord after SCI. To assess the functional role of Noggin, we used Results: As a result, we found that Noggin was upregulated in reactive astrocytes after SCI, suggesting its involvement in the injury response. Conditional deletion of Noggin markedly suppressed glial fibrillary acidic protein (GFAP) expression after SCI. Consistently, local administration of neutralizing anti-Noggin antibodies also reduced GFAP expression around the lesion site. However, anti-Noggin antibody treatment deteriorated motor function after SCI. Discussion: These findings suggest that Noggin is an important regulator of reactive astrogliosis and contributes to glial scar formation after SCI. Although suppression of Noggin reduced GFAP expression and attenuated glial scar formation, it did not improve functional recovery. Rather, motor function was worsened, indicating that reduced glial scar formation may not necessarily be beneficial after SCI. Noggin-mediated astrogliosis may therefore play a protective role in the injured spinal cord.
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