Abstract Rapid endothelialization is an effective way to treat intimal hyperplasia after intravascular stent implantation. Blood vessels and nerves coordinate with each other in function, while neurotrophin-3 (NT-3) is an important class of nerve growth factors. Our study found that NT-3 promoted endothelial progenitor cell (EPC) mobilization, and the proportion of EPCs in peripheral blood was increased by 1.774 times compared with the control group. Besides, NT-3 promoted the expression of stromal cell-derived factor-1α (SDF-1α), matrix metalloproteinase-9 (MMP9), and chemokine (C-X-C motif) receptor 4 (CXCR4) in EPCs, which increased by 59.89%, 74.46%, and 107.7%, respectively, compared with the control group. Transwell experiments showed that NT-3 enhanced the migration of EPCs by 1.31 times. Flow chamber experiments demonstrated that NT-3 captured more circulating EPCs. As shown by ELISA results, NT-3 can promote the paracrine of vascular endothelial growth factor, interleukin-8, MMP-9, and SDF-1 from EPCs. Such increased angiogenic growth factors further accelerated the closure of endothelial cell scratches. Additionally, EPC-conditioned medium in the NT-3 group significantly inhibited the proliferation of vascular smooth muscle cells. Then animal experiments also illustrated that NT-3 prominently accelerated the endothelialization of injured carotid artery. In short, NT-3 accelerated rapid reendothelialization of injured carotid artery through promoting EPC mobilization and homing.

中文翻译：

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Neurotrophin-3 通过诱导 EPC 动员和归巢加速再内皮化

摘要 快速内皮化是治疗血管内支架植入术后内膜增生的有效方法。血管和神经在功能上相互协调，而神经营养因子-3（NT-3）是一类重要的神经生长因子。我们的研究发现NT-3促进内皮祖细胞（EPC）动员，外周血中EPCs的比例较对照组增加1.774倍。此外，NT-3促进了EPCs中基质细胞衍生因子1α（SDF-1α）、基质金属蛋白酶9（MMP9）和趋化因子（CXC基序）受体4（CXCR4）的表达，增加了59.89%，与对照组相比分别为 74.46% 和 107.7%。Transwell 实验表明，NT-3 将 EPC 的迁移增强了 1.31 倍。流动室实验表明，NT-3 捕获了更多的循环 EPC。ELISA结果表明，NT-3可以促进EPCs分泌血管内皮生长因子、白细胞介素8、MMP-9和SDF​​-1。这种增加的血管生成生长因子进一步加速了内皮细胞划痕的闭合。此外，NT-3组的EPC条件培养基显着抑制血管平滑肌细胞的增殖。然后动物实验还表明NT-3显着加速了受伤颈动脉的内皮化。简而言之，NT-3 通过促进 EPC 动员和归巢加速受伤颈动脉的快速再内皮化。和来自 EPC 的 SDF-1。这种增加的血管生成生长因子进一步加速了内皮细胞划痕的闭合。此外，NT-3组的EPC条件培养基显着抑制血管平滑肌细胞的增殖。然后动物实验也表明NT-3显着加速了受伤颈动脉的内皮化。简而言之，NT-3 通过促进 EPC 动员和归巢加速受伤颈动脉的快速再内皮化。和来自 EPC 的 SDF-1。这种增加的血管生成生长因子进一步加速了内皮细胞划痕的闭合。此外，NT-3组的EPC条件培养基显着抑制血管平滑肌细胞的增殖。然后动物实验还表明NT-3显着加速了受伤颈动脉的内皮化。简而言之，NT-3 通过促进 EPC 动员和归巢加速受伤颈动脉的快速再内皮化。然后动物实验还表明NT-3显着加速了受伤颈动脉的内皮化。简而言之，NT-3 通过促进 EPC 动员和归巢加速受伤颈动脉的快速再内皮化。然后动物实验还表明NT-3显着加速了受伤颈动脉的内皮化。简而言之，NT-3 通过促进 EPC 动员和归巢加速受伤颈动脉的快速再内皮化。