Shear stress enhances human endothelial cell wound closure in vitro
Shear stress enhances human endothelial cell wound closure in vitro
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DOI：
10.1152/ajpheart.2000.279.1.h293
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发表时间：
2000-07-01
影响因子：
4.8
通讯作者：
Flozak, AS
中科院分区：
文献类型：
--
作者：
Albuquerque, MLC;Waters, CM;Flozak, AS
内皮的修复发生在持续血流的存在下，然而剪切力影响内皮伤口闭合的机制仍然难以捉摸。因此，我们测试了剪切应力增强内皮细胞伤口闭合的假设。人脐静脉内皮细胞（HUVEC）或人冠状动脉内皮细胞（HCAEC）在I型胶原包被的盖玻片上培养。在平行板流动室中以12 dyn/cm（2）剪切细胞单层18 h，以获得细胞排列，然后用金属刮刀刮伤。随后，在剪切-缠绕-剪切（S-W-sH）或剪切-缠绕-静态（S-W-sT）条件下，将单层暴露于3、12或20 dyn/cm（2）的层流剪切应力6 h。伤口闭合测量为原始伤口宽度的百分比。还测量了细胞面积、质心到质心距离和细胞速度。暴露于3、12或20 dyn/cm（2）的S-W-sH组的HUVEC伤口分别接近21、39或50%，而S-W-sT细胞中只有59%。类似地，HCAEC伤口闭合至29、49或33%（S-W-sH），而S-W-sT细胞中为58%。细胞扩散和迁移，而不是增殖，是伤口闭合率增加的主要机制。这些结果表明，生理水平的剪切应力增强内皮修复。
Repair of the endothelium occurs in the presence of continued blood flow, yet the mechanisms by which shear forces affect endothelial wound closure remain elusive. Therefore, we tested the hypothesis that shear stress enhances endothelial cell wound closure. Human umbilical vein endothelial cells (HUVEC) or human coronary artery endothelial cells (HCAEC) were cultured on type I collagen-coated coverslips. Cell monolayers were sheared for 18 h in a parallel-plate flow chamber at 12 dyn/cm(2) to attain cellular alignment and then wounded by scraping with a metal spatula. Subsequently, the monolayers were exposed to a laminar shear stress of 3, 12, or 20 dyn/cm(2) under shear-wound-shear (S-W-sH) or shear-wound-static (S-W-sT) conditions for 6 h. Wound closure was measured as a percentage of original wound width. Cell area, centroid-to-centroid distance, and cell velocity were also measured. HUVEC wounds in the S-W-sH group exposed to 3, 12, or 20 dyn/cm(2) closed to 21, 39, or 50%, respectively, compared with only 59% in the S-W-sT cells. Similarly, HCAEC wounds closed to 29, 49, or 33% (S-W-sH) compared with 58% in the S-W-sT cells. Cell spreading and migration, but not proliferation, were the major mechanisms accounting for the increases in wound closure rate. These results suggest that physiological levels of shear stress enhance endothelial repair.