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1 Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology/Emory University, Atlanta, Georgia, United States
2 Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology/Emory University, Atlanta, Georgia, United States; United States
* To whom correspondence should be addressed. E-mail: larry.mcintire{at}bme.gatech.edu.
The phenotype of endothelial cells (EC) is specific to the vascular bed from which they originate. To examine how mechanical forces alter the phenotype of different EC, 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%, 1Hz), to a motion control which simulated fluid agitation over the cells without strain, or to static conditions for 24 hrs. We measured H2O2 production using dichlorodihydrofluorescein acetate (DCFDA) and superoxide (O2
-) with dihydroethidium (DHE) 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 using Westerns. HUVEC under cyclic strain showed 1) higher intracellular H2O2 levels; 2) increased SOD, catalase, and GPx activities; and 3) greater vascular cell adhesion molecule (VCAM)-1 and intercellular adhesion molecule (ICAM)-1 protein expression, compared to 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. Opposite responses obtained with these two human endothelial cell types may reflect their vessels of origin, in that HAEC are subjected to higher cyclic strain deformations in vivo than HUVEC.
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