Abstract

Secondhand smoke (SHS) has been reported to affect endothelial cells (EC) activities, but it is unclear if this effect would be altered under flow conditions. The goal of this study was to investigate if EC from different vascular beds would respond to SHS differently under dynamic shear stress. Human coronary artery EC (HCAEC), human umbilical vein EC (HUVEC) and human pulmonary artery EC (HPAEC) were grown to confluence and treated with SHS extract overnight. Cells were then exposed to pulsatile shear stress (0.1–1 Pa) in a cone and plate shearing device for 1 hour at 37°C. EC activation was measured by cell surface ICAM‐1 expression using a solid phase ELISA approach. The results demonstrated that SHS increased cell surface ICAM‐1 expression significantly on HCAEC, but did not have much effect on HUVEC and HPAEC. After EC were exposed to dynamic shear stress, ICAM‐1 expression on HCAEC decreased to the level observed on untreated cells. No change was observed with HUVEC. For HPAEC, shear stress decreased ICAM‐1 expression significantly, compared to untreated cells. These results demonstrated that EC from different vascular beds respond to SHS differently, and SHS could be more damaging to EC located in coronary arteries. Physiological pulsatile shear stress could inhibit cell activation in HCAEC and HPAEC, suggesting its protective role for arterial EC. This work is support by OCAST HR10–027.

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