骨髓来源细胞(BMCs)参与脉络膜新生血管(CNV)的形成。近年来的研究多关注眼内移植BMCs在CNV的再生和修复作用。但BMCs在外周循环的数量有限，目前的技术和条件尚不能使体外扩增的BMCs被常规用于细胞治疗。已经证实调控CD26蛋白水解活动可降解和失活骨髓内的SDF-1，动员扩增体内的BMCs。我们近期的研究工作报道了CD26调控BMCs的一个亚群——内皮祖细胞(EPCs)的体内动员扩增，能够减轻CNV。因此我们推测，通过体内扩增BMCs能够提供充足的自体细胞，在CNV中发挥内源性的损伤修复作用。本课题拟在前期研究基础上，建立激光诱导的C57BL/6J-GFP嵌合体小鼠CNV 模型，利用FACS,WB, RT-RCR, ELISA及免疫荧光标记等方法，研究CD26调控BMCs在CNV血管损伤区可能的分化潜能及细胞治疗潜力，阐明具体的作用机制，为BMC细胞治疗CNV提供新的治疗策略。

The bone marrow-derived cells (BMCs) participate in choroidal neovascularization. In recent studies, much attention was paid to the repairing and regenerating functions of transplanting BMCs by intraocular injection in the pathological process of CNV. However, there are very limited BMCs in the peripheral circulation. Technology has not yet reached a stage where ex vivo-expanded BMCs can be routinely used for cell therapy. A recent finding has shown that SDF-1 degradation and inactivation within the bone marrow by CD26 may ultimately result in the mobilization and expansion of BMC. We has experimented and reported that a subgroup of cells in BMCs-endothelial precursor cells (EPCs)-could be mobilized and expanded by mediating CD26. In our results, we observed that the severity of CNV was decreased. Therefore, we hypothesized that enough autologous cells provided by expanding BMCs in vivo would play a repairing role in CNV. In this study, we plan to establish a C57BL/6J-GFP hybrid model of mouse by the laser-induced method. The roles and mechanisms of CD26 mediating BMCs in choroidal neovascularization will be studied through a diversity of ways, including FACS, WB, RT-RCR, ELISA etc. We believe the results of this study will equip us a new strategy of BMCs treating CNV finally.