Abstract
BackgroundExercise‐Induced Shear Stress (ESS) is characterized as a mechanical stimulus effecting cellular morphology and physiology. Varying ESS intensity elicit different response mechanisms through cellular signaling pathways. Higher intensity ESS enhances the expression of genes involved in protection against atherosclerosis. Adhesion molecules expression is common in atherosclerosis. Therefore, the purpose of this study was to determine the effects of different intensities of pulsatile ESS on vascular cell adhesion molecule‐1 (VCAM1) and intercellular adhesion molecule (ICAM1) gene expression.MethodsCommercially available human carotid artery endothelial cells (Sigma Aldrich) were cultured until 95–100% confluence and then exposed to pulsatile resting ESS (18 dynes/cm2) for 5 hours, followed by 1 hour low‐intensity ESS (35 dynes/cm2), or high‐intensity ESS (80 dynes/cm2) on parallel fluidic units (Ibidi, USA). Ibidi Pump Control Software (version 1.5.4, Ibidi, USA) was used to control shear stress intensity. mRNA was extracted and expression of VCAM1 and ICAM1 was assessed using qRT‐PCR. Samples were run in Changes in gene expression were calculated using the ΔΔ‐CT method, using GAPDH as the normalizing control gene. One‐way ANOVA was used to asses statistically significant differences (p < 0.05) using Prism version 8 (Graphpad).ResultsThe mRNA expression of VCAM1 and ICAM1 significantly increased (p <0.01). 6 and 8 folds respectively after exposure to low‐intensity ESS. Furthermore, high‐intensity ESS did not significantly increased the expression of VCAM1 and ICAM1.ConclusionLow‐intensity pulsatile exercise‐induced shear stress improves endothelial function in‐vitro through the increase in adhesion molecule’s gene expression.
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