数字农科院2.0

Epidermal Growth Factor Receptor-Extracellular-Regulated Kinase B.lockade Upregulates Trim32 Signaling C ascade And Promotes Neurogenesis After Spinal Cord Injury

文献类型： 外文期刊

作者： Xue, WW; Zhao, YN; Xiao, ZF; Wu, XM; Ma, DZ; Han, J; Li, X; Xue, XY; Yang, Y; Fang, YX; Fan, CX; Liu, SM; Xu, B; Han, SF; Chen, B; Zhang, HP; Fan, YH; Liu, WY; Dong, Q; Dai, JW

作者机构：

关键词： EGFR; myelin; neural stem cell; neurogenesis; neuronal differentiation; spinal cord injury

期刊名称： STEM CELLS

ISSN： 1066-5099

年卷期： 2019 年

页码：

收录情况： JCR（2021版）

摘要： Nerve regeneration is blocked after spinal cord injury (SCI) by a complex myelin-associated inhibitory (MAI) microenvironment in the lesion site; however, the underlying mechanisms are not fully understood. During the process of neural stem cell (NSC) differentiation, pathway inhibitors were added to quantitatively assess effects on neuronal differentiation. Immunoprecipitation and lentivirus-induced overexpression were used to examine effects in vitro. In vivo, animal experiments and lineage tracing methods were used to identify nascent neurogenesis after SCI. In vitro results indicated that myelin inhibited neuronal differentiation by activating the epidermal growth factor receptor (EGFR)-extracellular-regulated kinase (ERK) signaling cascade. Subsequently, we found that tripartite motif (TRIM) 32, a neuronal fate-determining factor, was inhibited. Moreover, inhibition of EGFR-ERK promoted TRIM32 expression and enhanced neuronal differentiation in the presence of myelin. We further demonstrated that ERK interacts with TRIM32 to regulate neuronal differentiation. In vivo results indicated that EGFR-ERK blockade increased TRIM32 expression and promoted neurogenesis in the injured area, thus enhancing functional recovery after SCI. Our results showed that EGFR-ERK blockade antagonized MAI of neuronal differentiation of NSCs through regulation of TRIM32 by ERK. Collectively, these findings may provide potential new targets for SCI repair.

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