title: Cyclic strain and motion control produce opposite oxidative responses in two human endothelial cell types.
abstract: The phenotype of endothelial cells (ECs) is specific to the vascular bed from which they originate. To examine how mechanical forces alter the phenotype of different ECs, we compared the effects of cyclic strain and motion control on reactive oxygen species (ROS) production and metabolism and cell adhesion molecule expression in human umbilical vein endothelial cells (HUVEC) vs. human aortic endothelial cells (HAEC). HUVEC and HAEC were subjected to cyclic strain (10% or 20%, 1 Hz), to a motion control that simulated fluid agitation over the cells without strain, or to static conditions for 24 h. We measured H(2)O(2) production with dichlorodihydrofluorescein acetate and superoxide with dihydroethidium fluorescence changes; superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx) activities spectrophotometrically; and vascular cell adhesion molecule (VCAM)-1 and intercellular adhesion molecule (ICAM)-1 protein expression with Western blot analyses. HUVEC under cyclic strain showed 1) higher intracellular H(2)O(2) levels, 2) increased SOD, catalase, and GPx activities, and 3) greater VCAM-1 and ICAM-1 protein expression, compared with motion control or static conditions. However, in HAEC, motion control induced higher levels of ROS, enzyme activities associated with ROS defense, and VCAM-1 and ICAM-1 expression than cyclic strain. The opposite responses obtained with these two human EC types may reflect their vessels of origin, in that HAEC are subjected to higher cyclic strain deformations in vivo than HUVEC.
authors.affiliation: Wallace H. Coulter Dept. of Biomedical Engineering, Georgia Institute of Technology, 313 Ferst Dr., Suite 2116, Atlanta, GA 30332-0535, USA.
authors.forename: Hak-Joon
authors.initials: HJ
authors.lastname: Sung
authors.forename: Andrew
authors.initials: A
authors.lastname: Yee
authors.forename: Suzanne G
authors.initials: SG
authors.lastname: Eskin
authors.forename: Larry V
authors.initials: LV
authors.lastname: McIntire
mesh_terms: D001011:Aorta / Q000166:cytology / Q000378:metabolism*; D002374:Catalase / Q000378:metabolism; D002448:Cell Adhesion; D015815:Cell Adhesion Molecules / Q000378:metabolism*; D048430:Cell Shape; D002478:Cells, Cultured; D042783:Endothelial Cells / Q000378:metabolism*; D005979:Glutathione Peroxidase / Q000378:metabolism; D006801:Humans; D006861:Hydrogen Peroxide / Q000378:metabolism; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D040542:Mechanotransduction, Cellular; D018384:Oxidative Stress; D010641:Phenotype; D011673:Pulsatile Flow; D017382:Reactive Oxygen Species / Q000378:metabolism*; D013314:Stress, Mechanical; D013482:Superoxide Dismutase / Q000378:metabolism; D013481:Superoxides / Q000378:metabolism; D014471:Umbilical Veins / Q000166:cytology / Q000378:metabolism*; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism
chemical_list: D015815:Cell Adhesion Molecules; D017382:Reactive Oxygen Species; D019010:Vascular Cell Adhesion Molecule-1; D013481:Superoxides; D018799:Intercellular Adhesion Molecule-1; D006861:Hydrogen Peroxide; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase