内毒素所致的微血管内皮损伤是多种危重疾病的病理基础，至今缺乏针对有效的治疗手段。已知内皮成集落祖细胞（ECFC）能在一定信号调控下"归巢"到损伤内皮发挥修复作用，但具体机制不明。我们在前期研究中发现内毒素性内皮损伤中，损伤内皮释放的e-selectin及其配体是调控ECFC归巢的重要胞外分子；而SDF-1a与其受体CXCR4结合后能促进ECFC的e-selectin配体的表达，但胞内调控途径不明。为此我们深入研究并发现C2GnT-1可能是ECFC胞内主要调控e-selectin配体合成的基因。结合文献报道我们提出C2GnT-1受SDF-1a/CXCR4信号途径调控的假设，并试图阐明这条胞内途径的机制。本研究拟通过体外研究、动物模型和临床研究初步阐明内毒素所致内皮损伤中调控ECFC归巢的胞内分子途径，对完善ECFC归巢功能的认识具有重要学术价值，也为治疗内毒素性内皮损伤提供潜在的新药靶点。

Endotoxin induced microvascular endothelial injury is a basic pathological process of many serious diseases. However,specific treatment is still absent. It is reported that endothelial colony forming cells(ECFC) can help to repair endothelial injury by homing to injured endothelial following specific molecules, but the mechanism is still undefined. In our previous study, we find that e-selectin produced by impaired endothelial cells takes part in regulating the homing of ECFC during endotoxin induced endothelial injury. SDF-1a contributes to expressing the ligands of e-selectin by binding to its ligand CXCR4, but the endocellular mechanism is unknown.Our further research proposes that C2GnT-1, which is supposed to be regulated by SDF-1a/CXCR4, may play a role in regulating the synthesis of e-selectin ligands. This project is expected to clarify the mechanism of the ECFC homing in vitro and in vivo,which will contribute to the EPC homing research and also offer potent theraputic targets on endotoxic endotheial injury.