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Overexpression of Foxc1 regenerates crushed rat facial nerves by promoting Schwann cells migration via the Wnt/β-catenin signaling pathway.
Journal of Cellular Physiology ( IF 4.5 ) Pub Date : 2020-05-11 , DOI: 10.1002/jcp.29772 Wenzheng Xia 1 , Jin Zhu 1 , Xueyi Wang 1 , Yinda Tang 1 , Ping Zhou 1 , Xiangyu Wei 1 , Bowen Chang 1 , Xuan Zheng 1 , Wanchun Zhu 1 , Meng Hou 2 , Shiting Li 1
Journal of Cellular Physiology ( IF 4.5 ) Pub Date : 2020-05-11 , DOI: 10.1002/jcp.29772 Wenzheng Xia 1 , Jin Zhu 1 , Xueyi Wang 1 , Yinda Tang 1 , Ping Zhou 1 , Xiangyu Wei 1 , Bowen Chang 1 , Xuan Zheng 1 , Wanchun Zhu 1 , Meng Hou 2 , Shiting Li 1
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Facial paralysis can result in severe implications for patients. A good prognosis depends on the degree of nerve regeneration. Schwann cells (SCs) play an important role in facial nerve development and regeneration through migration. Forkhead box C1 (Foxc1), a member of the forkhead transcription factor family, is implicated in cell migration. However, the role of Foxc1 in the progression after facial nerve crush remains unknown. Our aim was to evaluate the effect of Foxc1 overexpression on SC migration and recovery of facial nerves after crush injury. The rat facial nerve crush injury model was established through the use of unilateral surgery. The results showed that the expression of Foxc1 was increased in the surgery group compared to that of the control group. SCs were isolated from the sciatic nerves and cultured. Foxc1, delivered by an adeno‐associated virus in vivo, or adenovirus in vitro, both induced overexpression of Foxc1, and increased the expression of CXCL12 and β‐catenin. After the transfection of Foxc1, the migration of SC was increased both in vitro and in vivo, was reduced by the inhibition of CXCL12 or β‐catenin. The facial nerve function and the nerve axon remyelination of the rats transfected with Foxc1 were significantly improved after nerve crush injury. Overall, the results demonstrated that overexpression of Foxc1 promoted SC migration by regulating CXCL12 via the Wnt/β‐catenin pathway, thus contributing to improved facial nerve function after crush injury.
中文翻译：
Foxc1的过表达通过促进经由Wnt /β-catenin信号传导途径的雪旺细胞迁移来再生被压迫的大鼠面神经。
面瘫可能对患者造成严重影响。良好的预后取决于神经再生的程度。雪旺细胞（SCs）在面神经发育和通过迁移再生中起重要作用。叉头盒C1（Foxc1）是叉头转录因子家族的成员，与细胞迁移有关。但是，Foxc1在面部神经挤压后进展中的作用仍然未知。我们的目的是评估Foxc1过表达对挤压伤后面神经SC迁移和恢复的影响。通过单侧手术建立大鼠面神经挤压伤模型。结果表明，与对照组相比，手术组Foxc1的表达增加。从坐骨神经分离SC并进行培养。Foxc1，体内由腺相关病毒或体外腺病毒介导的病毒均诱导Foxc1过表达，并增加CXCL12和β-catenin的表达。Foxc1转染后，SC的迁移在体内和体外均增加，并通过抑制CXCL12或β-catenin而减少。神经挤压伤后转染Foxc1的大鼠的面神经功能和神经轴突髓鞘再生明显改善。总体而言，结果表明，Foxc1的过表达通过Wnt /β-catenin途径调节CXCL12促进了SC迁移，从而有助于改善挤压伤后的面神经功能。在体外和体内，SC的迁移都增加了，而通过抑制CXCL12或β-catenin减少了SC的迁移。神经挤压伤后转染Foxc1的大鼠的面神经功能和神经轴突髓鞘再生明显改善。总体而言，结果表明，Foxc1的过表达通过Wnt /β-catenin途径调节CXCL12促进了SC迁移，从而有助于改善挤压伤后的面神经功能。在体外和体内，SC的迁移都增加了，而通过抑制CXCL12或β-catenin减少了SC的迁移。神经挤压伤后转染Foxc1的大鼠的面神经功能和神经轴突髓鞘再生明显改善。总体而言，结果表明，Foxc1的过表达通过Wnt /β-catenin途径调节CXCL12促进了SC迁移，从而有助于改善挤压伤后的面神经功能。
更新日期：2020-05-11
中文翻译：
Foxc1的过表达通过促进经由Wnt /β-catenin信号传导途径的雪旺细胞迁移来再生被压迫的大鼠面神经。
面瘫可能对患者造成严重影响。良好的预后取决于神经再生的程度。雪旺细胞（SCs）在面神经发育和通过迁移再生中起重要作用。叉头盒C1（Foxc1）是叉头转录因子家族的成员，与细胞迁移有关。但是，Foxc1在面部神经挤压后进展中的作用仍然未知。我们的目的是评估Foxc1过表达对挤压伤后面神经SC迁移和恢复的影响。通过单侧手术建立大鼠面神经挤压伤模型。结果表明，与对照组相比，手术组Foxc1的表达增加。从坐骨神经分离SC并进行培养。Foxc1，体内由腺相关病毒或体外腺病毒介导的病毒均诱导Foxc1过表达，并增加CXCL12和β-catenin的表达。Foxc1转染后，SC的迁移在体内和体外均增加，并通过抑制CXCL12或β-catenin而减少。神经挤压伤后转染Foxc1的大鼠的面神经功能和神经轴突髓鞘再生明显改善。总体而言，结果表明，Foxc1的过表达通过Wnt /β-catenin途径调节CXCL12促进了SC迁移，从而有助于改善挤压伤后的面神经功能。在体外和体内，SC的迁移都增加了，而通过抑制CXCL12或β-catenin减少了SC的迁移。神经挤压伤后转染Foxc1的大鼠的面神经功能和神经轴突髓鞘再生明显改善。总体而言，结果表明，Foxc1的过表达通过Wnt /β-catenin途径调节CXCL12促进了SC迁移，从而有助于改善挤压伤后的面神经功能。在体外和体内，SC的迁移都增加了，而通过抑制CXCL12或β-catenin减少了SC的迁移。神经挤压伤后转染Foxc1的大鼠的面神经功能和神经轴突髓鞘再生明显改善。总体而言，结果表明，Foxc1的过表达通过Wnt /β-catenin途径调节CXCL12促进了SC迁移，从而有助于改善挤压伤后的面神经功能。
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