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血管内皮细胞迁移和黏附对支架再内皮化的联合作用

The Combined Contribution of Vascular Endothelial Cell Migration and Adhesion to Stent Re-endothelialization.

作者信息

Wang Xiaoli, Fang Fei, Ni Yinghao, Yu Hongchi, Ma Jia, Deng Li, Li Chunli, Shen Yang, Liu Xiaoheng

机构信息

West China School of Basic Medical Sciences and Forensic Medicine, Institute of Biomedical Engineering, Sichuan University, Chengdu, China.

出版信息

Front Cell Dev Biol. 2021 Mar 4;9:641382. doi: 10.3389/fcell.2021.641382. eCollection 2021.

Abstract

Coronary stent placement inevitably causes mechanical damage to the endothelium, leading to endothelial denudation and in-stent restenosis (ISR). Re-endothelialization depends mainly on the migration of vascular endothelial cells (VECs) adjacent to the damaged intima, as well as the mobilization and adhesion of circulating VECs. To evaluate the combined contribution of VEC migration and adhesion to re-endothelialization under flow and the influence of stent, models were constructed to simulate various endothelial denudation scales (2 mm/5 mm/10 mm) and stent deployment depths (flat/groove/bulge). Our results showed that (1) in 2 mm flat/groove/bulge models, both VEC migration and adhesion combined completed the percentage of endothelial recovery about 27, 16, and 12%, and migration accounted for about 21, 15, and 7%, respectively. It was suggested that the flat and groove models were in favor of VEC migration. (2) With the augmentation of the injury scales (5 and 10 mm), the contribution of circulating VEC adhesion on endothelial repair increased. Taken together, endothelial restoration mainly depended on the migration of adjacent VECs when the injury scale was 2 mm. The adhered cells contributed to re-endothelialization in an injury scale-dependent way. This study is helpful to provide new enlightenment for surface modification of cardiovascular implants.

摘要

冠状动脉支架置入不可避免地会对内皮造成机械损伤,导致内皮剥脱和支架内再狭窄(ISR)。再内皮化主要依赖于受损内膜附近血管内皮细胞(VECs)的迁移,以及循环VECs的动员和黏附。为了评估VEC迁移和黏附在血流状态下对再内皮化的综合贡献以及支架的影响,构建了模型来模拟各种内皮剥脱尺度(2毫米/5毫米/10毫米)和支架展开深度(平面/凹槽/凸起)。我们的结果表明:(1)在2毫米平面/凹槽/凸起模型中,VEC迁移和黏附共同完成的内皮恢复百分比分别约为27%、16%和12%,迁移分别占约21%、15%和7%。提示平面和凹槽模型有利于VEC迁移。(2)随着损伤尺度增大(5毫米和10毫米),循环VEC黏附对内皮修复的贡献增加。综上所述,当损伤尺度为2毫米时,内皮修复主要依赖于相邻VECs的迁移。黏附细胞以损伤尺度依赖的方式促进再内皮化。本研究有助于为心血管植入物的表面改性提供新的启示。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de73/7969796/c485331bcd62/fcell-09-641382-g001.jpg

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