内皮细胞修复滞后是经皮冠状动脉介入治疗（PCI）术后支架内血栓形成的主要原因，其确切发生机制尚未阐明。我们前期实验发现丝氨酸蛋白酶家族成员二肽基肽酶-4（DPP-4）活性下调具有抑制血管损伤后血管内膜增生的作用。体内DPP-4活性抑制通过上调SDF-1α表达从而促进内皮祖细胞动员参与血管损伤后修复。因此本课题假设：血管机械性损伤后，体内DPP-4活性升高诱导Ephrin-B2与SDF-1α/CXCR4竞争性激活下游转录因子，促细胞致密外周束生成而抑制细胞纤维型肌动蛋白生成，迟滞内皮细胞迁移修复。为证实这一假说，我们将复制SD鼠颈动脉球囊损伤模型，通过血管功能学实验和分子生物学等技术，从整体-组织-细胞三个水平，证明DPP-4活性升高是PCI术后由支架内内皮修复障碍导致血栓形成的主要原因。本课题将从新的视角阐明PCI术后内皮修复滞后的分子机制，并为其防治提供新靶点。

Delate endothelialization is the main reason which will lead to the formation of thrombosis after percutaneous coronary interventions. Ourprevious research conform that inhibit the expression DPP-4 which belong to the serine protease family has the ability to reverse the process of intimal hyperplasia. Decrease the activity of DPP-4 can stimulate the expression of SDF-1α, and then mobilize the endothelial progentior cell. Therefore we hypothesize that increase the activity of DPP-4 is closely related to change the balance between Ephrin-B2 and SDF-1α/CXCR4 to regulate the expression of transcription factor in respond to the synthesis of dense peripheral band and F-actin in endothelial cell, prohibit the migration of endothelial cell. We will use balloon injury model, vascular function studies and molecular biology techniques determine the signaling pathway by which increase the activity of DPP-4 play important role in regulate the recovery of EC which lead to the thrombosis formation after PCI. This project will put forward new sight and potential therapeutic target to treatment delate endothelialization after PCI.