间充质干细胞（MSC）较强的自我更新和多向分化潜能为诱导毛发再生提供了可能，然而移植后较低的迁移和归巢效率限制了其应用。链接粘附分子JAM1是介导造血干细胞及淋巴细胞归巢的关键分子，其对MSC迁移和归巢的影响目前尚无报道。我们在前期研究中证明MSC可以分化为毛乳头和毛囊上皮细胞，促进裸鼠的毛发再生，进一步通过慢病毒转染上调JAM1基因后发现MSC迁移能力增强，移植后JAM1ov-MSC趋化归巢到裸鼠毛囊的数量增多，促进了毛囊结构重建和毛发再生，基于此，我们推测JAM1基因修饰可以增强MSC趋化归巢至损伤组织的能力，促进损伤器官修复和毛发再生。本研究拟以毛发缺失的裸鼠为模型，探讨JAM1基因修饰促进MSC迁移归巢的可能机制，在此基础上探寻MSC增强毛发再生能力的新途径，为我们治疗毛发再生提供新思路。

Recent advances in stem cell research have suggested that transplantion of mesenchymal stem cells (MSC) possess therapeutic potential for hair regeneration, but the low efficiency of MSC homing after transplantion still exist. The junctional adhesion molecule 1 (JAM1) has been shown to serve a crucial role in hematopoietic stem cell and lymphocytes, there no report on the JAM1' impact of the MSC homing.In preliminary studies,we have proved that human early embryo-derived MSC(hMSC) can induce hair regrowth in nude mice. Furthermore, lentiviral infection and cell migration was used and we found that the JAM1 over expression hMSC(JAM1ov-MSC) has increased migration and proliferation ability. In view of the number of JAMov-MSC migration to hair follicle(HF) was increased in animal experiments, we hypothesized that JAM1ov-MSC play an important role in har regenetation.We intend to utilize nude mice as hair missing animal models to carry out hair regeneration study. Migration and homing of JAM1ov-MSC is research focus. In vitro, cultured cell migration model is used to testify the activated signaling channels of JAM1.