An EGFR inhibitor induces Schwann cell proliferation and promotes functional recovery with remyelination in injured peroneal nerve after end-to-side neurorrhaphy

EGFR 抑制剂诱导雪旺细胞增殖并促进端侧神经缝合术后受损腓神经髓鞘再生的功能恢复

• 批准号: 23592160
• 负责人: WAKABAYASHI YOSHIAKI
• 金额: $ 3.16万
• 依托单位: Tokyo Medical and Dental University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2011
• 资助国家: 日本
• 起止时间: 2011 至 2013
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23592160/
• 关键词: 神経再生; 上皮成長因子受容体; 神経栄養因子; 末梢神経損傷; 再生; シュワン細胞

In this study, we tested whether the inhibition of epidermal growth factor receptor (EGFR) regulates neurite extension in DRG neurons or Schwann cell (SC) proliferation in vitro and nerve regeneration in injured proneal nerves after end-to-side neurorrhaphy (ETS). The in vitro results showed that regeneration of neurites from explanted DRG neurons was not significantly accelerated by administration of EGFR inhibitor (EGFI). In contrast, the number of SCs was increased with EGFI treatment as shown by a viability assay. Rat peroneal nerve was cut and then ETS was performed 3 weeks later. EGFI was infused by osmotic pump at the injury site for 7 days. After the surgery, motor score was increased significantly at 2 weeks and the amount of myelin in the peroneal nerve was increased significantly at 4 weeks in the EGFI infusion group. These findings suggest that local administration of EGFI has the potential to increase functional recovery after peripheral nerve injury.

在这项研究中，我们测试了表皮生长因子受体（EGFR）的抑制是否调节DRG神经元或许旺细胞（SC）的体外增殖和端侧神经吻合术（ETS）后受损的腓神经的神经再生的轴突延伸。体外实验结果表明，EGFR抑制剂（EGFI）不能明显促进DRG神经元突起的再生。相反，如活力测定所示，EGFI处理增加了SC的数量。切断大鼠腓总神经，3周后行ETS。EGFI通过渗透泵注入损伤部位7天。术后2周时运动评分显著增加，4周时EGFI灌注组腓神经中髓鞘含量显著增加。这些发现表明，局部给予EGFI有可能增加周围神经损伤后的功能恢复。

项目成果

東京医科歯科大学整形外科

东京医科齿科大学骨科