Abstract
Purpose: To determine whether exercise-induced levels of endothelial shear stress (ESS) observed in vivo upregulates endothelial protective proteins in vitro. Methods: In vivo carotid ESS was obtained from previously published data. Human umbilical vein endothelial cells were seeded in a collagen-coated Y-luer slides with a bifurcation that mimics the common carotid artery and its bifurcation. Four duplicate groups were exposed to 5 hours of resting ESS (18 dynes/cm2) followed by 1 hour of ESS at 18 dynes/cm2 × heart rate (HR) 60 pulses per minute (ppm) (control), 35 dynes/cm2 × HR 100 ppm (low), 50 dynes/cm2 × HR 120 ppm (moderate), or 60 dynes/cm2 × HR 150 ppm (high). After ESS exposure, cells were stained to identify cell nucleus, phosphorylated endothelial NO synthase (eNOSp), and intracellular actin concentrations using immunohistochemistry. Confocal microscopy images captured areas exposed to varying degrees of shear stress within the “common” artery, the bifurcation, and the distal branches of the bifurcation. Results: Images showed a higher expression of eNOSp and actin that is generally intensity and location dependent. High shear stress (HSS) showed the greatest eNOSp expression compared with all conditions at the after-bifurcation site (P < .05). Interestingly, HSS continued to result in greater expression of actin at the bifurcation site across all 4 intensities, where blood flow is known to be more turbulent. Conclusions: These findings may support the hypothesis that high shear stress plays an important protective endothelial role in relation to individualized exercise prescription as a contribution to precision medicine. Impact Statement: Endurance exercise intensity has a direct impact in endothelial cell homeostasis at the physiological and molecular levels. When a physical therapist prescribes endurance exercise for cardiovascular diseases, the goal should be to deliver precision medicine to enhance patient's health outcomes.
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