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Effects of Laminar Shear Stress on Race‐dependent Oxidative Stress Responses in Human Umbilical Vein Endothelial Cells
Author(s) -
Feairheller Deborah L,
Park JoonYoung,
Sturgeon Kathleen M,
Kim Boa,
Brown Michael D
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.831.6
Subject(s) - umbilical vein , oxidative stress , shear stress , laminar flow , stress (linguistics) , chemistry , biology , endocrinology , materials science , biochemistry , mechanics , composite material , physics , linguistics , philosophy , in vitro
We have previously shown that African American (AA) HUVECs have heightened oxidative stress levels compared to Caucasian (C) HUVECs. In vivo , vascular endothelial cells undergo a constant flow‐mediated laminar shear stress (LSS) from flowing blood. Aerobic exercise increases blood flow and thus the shear force on endothelial cells which increases NO production, modulates vascular tone, and decreases oxidative stress. We examined whether there were race‐dependent responses in NO production, antioxidant activity, and oxidative stress through NADPH oxidase to LSS. HUVECs were grown in parallel and then subjected to LSS at low (5dyne/cm 2 ) and high (20dyne/cm 2 ) levels for 24hrs. High LSS in AA HUVECs caused a 2 fold reduction in NADPH oxidase subunits p47phox, NOX2, and NOX4, a 2–5 fold increase in superoxide dismutase (SOD)‐2, Catalase, and eNOS expressions, and a 2–3 fold increase in NO production, total antioxidant and SOD activity. Smaller but similar responses were seen to low LSS. For C HUVECs, high LSS also caused a 1–5 fold increase in SOD2, Catalase, and eNOS, but caused only a reduction in NOX4 protein expression. It appears that AA HUVECs have a larger response to LSS indicating that aerobic exercise prescriptions may be valuable for this population because the potential exists for larger improvements. NIH/NHLBI RO1 HL085497 & NIH/NIA KO1 AG019640