新生血管性角膜病是常见的致盲性眼病，但不同病因导致的角膜新生血管在生长方式上差异很大，临床治疗棘手。我们前期研究发现：角膜基质微环境的变化在角膜新生血管形成中起着关键性作用，阻断Notch信号影响了角膜新生血管的生长方式。有研究发现RBP-J条件敲除小鼠角膜有自发新生血管形成，并伴有角膜基质结构的变化。RBP-J是Notch信号通路调控肿瘤和视网膜新生血管形成中Tip/Stalk细胞"命运选择"的关键"中枢"因子，但角膜基质微环境是否可通过影响血管内皮细胞Notch/RBP-J通路，调控角膜新生血管不同的生长方式尚不清楚。本课题拟采用正常和RBP-J条件敲除小鼠，建立碱烧伤等角膜新生血管模型，结合细胞和分子生物学方法，比较研究两种小鼠角膜基质微环境对血管内皮细胞Notch/RBP-J信号通路活化影响的异同，阐明其调控角膜新生血管生长方式的分子机制，为角膜新生血管的干预和治疗提供新的靶点。

Corneal neovascularization is a common cause of corneal blindness. However, the growth patterns assumed significant differences among different etiology. The unclear mechanisms cause the difficulty of clinical treatment. Our preliminary results found that the changes of stromal microenvironment played a critical role in corneal neovascularization, RBP-J conditional knock-out mice have spontaneous corneal neovascularization and stromal structure changes, while the blocking of Notch signaling affected the growth pattern of corneal neovascularization. The results indicate Notch/RBP-J signaling pathway may be involved in regulating the formation and growth pattern of corneal neovascularization, but the regulatory mechanism remains unclear. The present study intends to investigate the mechanisms of the interactions between stromal microenvironment and Notch/RBP-J signaling in corneal neovascularization, by using the RBP-J conditional knockout mice and corneal neovascularization model. The purpose is to provide new targets of corneal neovascularization intervention and treatment.