光感受器前体细胞移植为视网膜退行性疾病提供了新的治疗手段，移植细胞能否迁移至损伤部位是需要攻克的一大难题。我们曾报道视网膜Müller细胞源性光感受器样细胞（MC-PCs）可成为修复视网膜损伤的新的种子细胞，但MC-PCs注入光感受器损伤模型鼠的视网膜下腔后，仅部分迁移至损伤位点，我们在预实验中发现Reelin可提高MC-PCs的体外和体内的迁移能力；根据RNA-Seq、生物信息学分析以及Western blot结果，推测Reelin通过激活ERK信号增强了MC-PCs的迁移能力。为验证以上假说，本研究拟通过细胞水平和光感受器损伤模型鼠两个层面，采用基因沉默、Western blot、qPCR等一系列分子生物学技术阐明Reelin促进MC-PCs迁移的具体分子机制，为视网膜退行性疾病的细胞移植治疗提供新的思路及辅助方法。

Photoreceptor precursor cells transplantation provides a new treatment for retinal degenerative diseases, Whether the transplanted cells can migrate to the site of injury is a difficult problem that needs to be tackled. We have reported that retinal Müller cells-derived photoreceptor-like cells (MC-PCs) can be used as new seed cells for repairing retinal damage. However,when the differentiated photoreceptor precursor cells were injected into the subretinal space of the photoreceptor injured model of rat, partial cells migrated to the injury site. We found in preliminary experiments that Reelin increased the migration rates of transplanted cells in vitro and in vivo; Based on RNA-Seq、 bioinformatics analysis and Western blot, We speculate that Reelin enhances the migration ability of MC-PCs by activating ERK signaling pathway. To verify the above hypothesis, a series of molecular biological techniques such as gene silencing，Western blot, qPCR and so on will be used to analyze the mechanisms of Reelin promoting the migration of MC-PCs,which will provide a new avenue for cell transplantation therapy for retinal degenerative diseases.