Reendothelialisation is the natural pathway that inhibits neointimal hyperplasia and in-stent restenosis. Circulating endothelial progenitor cells (EPCs) derived from bone marrow (BM) might contribute to endothelial repair. However, the temporal and spatial distributions of reendothelialisation and neointimal hyperplasia after EPC transplantation in injured arteries are currently unclear. A carotid balloon injury (BI) model was established in Sprague-Dawley rats, and PKH26-labelled BM-derived EPCs were transplanted after BI. The carotid arteries were harvested on the first, fourth, seventh, and 14th day post-injury and analysed via light-sheet fluorescence microscopy and pathological staining (n = 3). EPC and human umbilical vein endothelial cell culture supernatants were collected, and blood samples were collected before and after transplantation. The paracrine effects of VEGF, IGF-1, and TGF-β1 in cell culture supernatants and serum were analysed by enzyme-linked immunosorbent assay (n = 4). Transplanted EPCs labelled with PKH26 were attached to the injured luminal surface the first day after BI. In the sham operation group, the transplanted EPCs did not adhere to the luminal surface. From the fourth day after BI, the mean fluorescence intensity of PKH26 decreased significantly. However, reendothelialisation and inhibition of neointimal hyperplasia were significantly promoted by transplanted EPCs. The degree of reendothelialisation of the EPC7d and EPC14d groups was higher than that of the BI7d and BI14d groups, and the difference in neointimal hyperplasia was observed between the EPC14d and BI14d groups. The number of endothelial cells on the luminal surface of the EPC14d group was higher than that of the BI14d group. The number of infiltrated macrophages in the injured artery decreased in the EPC transplanted groups. Transplanted EPCs had chemotactic enrichment and attached to the injured arterial luminal surface. Although decreasing significantly after the fourth day at the site of injury after transplantation, transplanted EPCs could still promote reendothelialisation and inhibit neointimal hyperplasia. The underlying mechanism is through paracrine cytokines and not differentiation into mature endothelial cells.

中文翻译：

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内皮祖细胞移植对大鼠颈动脉球囊导管损伤后新内膜增生和再内皮化的影响

内皮细胞增生是抑制新内膜增生和支架内再狭窄的天然途径。源自骨髓（BM）的循环内皮祖细胞（EPC）可能有助于内皮修复。然而，目前尚不清楚EPC移植后在受伤的动脉中内皮再形成和新内膜增生的时间和空间分布。在Sprague-Dawley大鼠中建立颈动脉球囊损伤（BI）模型，并在BI后移植PKH26标记的BM来源的EPC。在受伤后的第一天，第四天，第七天和第14天收获颈动脉，并通过光片荧光显微镜和病理染色进行分析（n = 3）。收集EPC和人脐静脉内皮细胞培养上清液，并在移植前后收集血液样品。通过酶联免疫吸附试验（n = 4）分析了VEGF，IGF-1和TGF-β1在细胞培养上清液和血清中的旁分泌作用。BI后第一天，将标记有PKH26的EPC移植到受损的腔表面。在假手术组中，移植的EPC未粘附在腔表面上。从BI后的第四天开始，PKH26的平均荧光强度显着下降。然而，移植的EPCs显着促进了内皮内皮化和新内膜增生的抑制。EPC7d和EPC14d组的血管内皮增生程度高于BI7d和BI14d组，并且在EPC14d和BI14d组之间观察到新内膜增生的差异。EPC14d组腔表面的内皮细胞数量高于BI14d组。EPC移植组受伤动脉中浸润的巨噬细胞数量减少。移植的EPC具有趋化富集，并附着在受损的动脉腔表面。尽管在移植后第四天在受伤部位明显减少，但移植的EPC仍可促进内皮细胞再生并抑制新内膜增生。潜在的机制是通过旁分泌细胞因子，而不是分化为成熟的内皮细胞。尽管在移植后第四天在受伤部位明显减少，但移植的EPC仍可促进内皮细胞再生并抑制新内膜增生。潜在的机制是通过旁分泌细胞因子，而不是分化为成熟的内皮细胞。尽管在移植后第四天在受伤部位明显减少，但移植的EPC仍可促进内皮细胞再生并抑制新内膜增生。潜在的机制是通过旁分泌细胞因子，而不是分化为成熟的内皮细胞。