Shear stress enhances human endothelial cell wound closure in vitro

Repair of the endothelium occurs in the presence of continued blood flow, y et the mechanisms by which shear forces affect endothelial wound closure re main elusive. Therefore, we tested the hypothesis that shear stress enhance s endothelial cell wound closure. Human umbilical vein endothelial cells (H UVEC) or human coronary artery endothelial cells (HCAEC) were cultured on t ype 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 monola yers 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. Cel l 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 cell s. 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 proliferatio n, were the major mechanisms accounting for the increases in wound closure rate. These results suggest that physiological levels of shear stress enhan ce endothelial repair.