血管系统的生成是脊椎动物器官发生中的最早进程之一，其对胚胎和胎儿的正常发育有着至关重要的影响。近来，细胞自噬在胚胎器官形成中细胞重塑功能的研究越来越多，但细胞自噬在血管系统生成中的作用尚不完全明确。我们的前期研究发现ATG7等多个自噬基因表达在早期胚胎血管发生的不同阶段，且自噬干扰剂处理鸡胚及自噬相关信号的转基因鼠模型血管发育不良，提示自噬在胚胎早期血管系统生成中发具有重要的作用。本研究，我们将以ATG7-/-、p110δ-/-等基因敲除鼠，STZ诱导糖尿病鼠和鸡胚为模型，按照血管系统生成的时程（血管发生和血管新生），利用Time lapse、原位杂交、免疫荧光、qRT-PCR、Western blot以及Microarray等技术研究自噬调控血管生成的基因功能学机制，揭示正常生理和应激状态下，细胞自噬在胚胎早期血管系统生成中的作用，为先天性血管生成不良导致的疾病及流产提供理论和实验依据。

Vasculature formation, which is one of the earliest processes of vertebrate organogenesis, plays the important role in the embryo and fetal development. Recently, the accumulating data indicated the role of cell autophagy on cell remodeling during embryonic organogenesis. However, the role of autophagy in the vasculature formation has still been obscure. In our previous study, we found that autophagy-related genes including ATG7 were expressed in the vascular system of early developing embryos. The angiodysplasia could be found following the treatment of autophagy interference agent in chick embryos. Likewise, placental vascular dysplasia occurred at autophagy-related gene knock-out mice. All of these data suggests that autophagy plays an important role in early embryonic vasculature formation. In this study, we would like to employ ATG7-/- (or conditional KO mice based on the experimental progress) or p110δ-/- knock-out mice and autophagy-interfered chick embryos to investigate the expression pattern of autophagy-related genes and the crucial angiogenesis-related genes during vasculature formation under normal physiological conditions, or stress state according to the chronological order of vasculature formation (vasculogenesis and angiogenesis) using in situ hybridization and immunofluorescence, qRT-PCR and Western blot, microarray, real time-lapse recording respectively. These experimental data would reveal the precise role of autophagy during differential stages of vasculature formation, and provide theoretical and experimental basis for congenital disease and abortion caused by angiodysplasia.