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Am J Physiol Heart Circ Physiol 279: H293-H302, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 1, H293-H302, July 2000

Shear stress enhances human endothelial cell wound closure in vitro

Maria Luiza C. Albuquerque1, Christopher M. Waters2,3,4, Ushma Savla2,3,4, H. William Schnaper1, and Annette S. Flozak1

Departments of 1 Pediatrics, 2 Anesthesia and 3 Medicine, Northwestern University Medical School, and 4 Department of Biomedical Engineering, Northwestern University School of Engineering, Chicago, Illinois 60611

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/cm2 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/cm2 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/cm2 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.

vasculature; biomechanics; intimal healing; cell migration; cell spreading


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