Abstract
BackgroundReendothelialisation 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.MethodsA 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).ResultsTransplanted 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.ConclusionsTransplanted 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.
Highlights
Reendothelialisation is the natural pathway that inhibits neointimal hyperplasia and in-stent restenosis
The underlying mechanism is through paracrine cytokines and not differentiation into mature endothelial cells
The effect of Endothelial progenitor cell (EPC) transplantation on neointimal hyperplasia in balloon injury (BI) carotid arteries The neointimal volume increased from BI1d, BI4d, BI7d, to BI14d
Summary
Reendothelialisation is the natural pathway that inhibits neointimal hyperplasia and in-stent restenosis. The injured vascular endothelium can cause vascular inflammation, which accelerates lipid deposition and thrombosis. These changes contribute to neointimal hyperplasia and in-stent restenosis (ISR) [3, 4]. Reendothelialisation is a natural pathway that inhibits neointimal hyperplasia and ISR. Circulating EPCs may accelerate reendothelialisation by paracrine signalling and differentiate into mature VECs [9, 10]. EPCs in culture after 14–28 days should be identified as non-haematopoietic EPCs. EPCs in culture after 14–28 days should be identified as non-haematopoietic EPCs These cells could replace and differentiate into mature VECs [20,21,22]. The temporal and spatial distributions of reendothelialisation and neointimal hyperplasia of injured arteries after EPC transplantation are currently unclear
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