Frontiers in neural circuits · 2026
Loss of function of Noggin inhibits glial scar formation and motor function recovery after spinal cord injury.
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Han Yibo, Wakayama Yuki, Li Shuo, Liang Dong, Li Juntan, Ping Yashuang, Arima Hideyuki, Sato Kohji, Matsuyama Yukihiro, Yamagishi Satoru
Аннотация
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 Nestin-Cre; Nogginflox/flox conditional knockout mice, in which Noggin is conditionally deleted from astrocytes and neurons in the spinal cord. In addition, neutralizing anti-Noggin antibodies were continuously administered to the lesion site using micro-osmotic pumps. GFAP expression and motor function after SCI were then evaluated.
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.
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 Nestin-Cre; Nogginflox/flox conditional knockout mice, in which Noggin is conditionally deleted from astrocytes and neurons in the spinal cord. In addition, neutralizing anti-Noggin antibodies were continuously administered to the lesion site using micro-osmotic pumps. GFAP expression and motor function after SCI were then evaluated.
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.