Abstract
The human saphenous vein (HSV) is commonly used in coronary artery bypass grafts. The patency of the vein graft in an arterial environment is limited, thereby requiring a high percentage of autograft recipients to repeat the bypass surgery within 5 years. The main problem that ensues with HSV grafts is due to the development of intimal hyperplasia (IH) which compromises vessel function. The mechanistic reasons for the development of IH and limited HSV patency are not currently understood. However, it has been proposed that the change from venous to arterial shear stress may be a trigger. Aquaporin 1 (AQP1), a water channel protein, is expressed in the plasma membrane of vascular endothelial cells. It is hypothesized that enhanced AQP1 expression may be an early biomarker for the development of IH. The goal of this study was to assess the effect of shear stress on AQP1 expression in cultured endothelial cells. Primary vascular endothelial cells seeded on a gelatin‐coated Ibidi flow chamber grown in static conditions expressed low levels of AQP1 protein that localized around the nucleus. In contrast, AQP1 was present in vesicles throughout the cytoplasm in increasing abundance in cells subjected to low shear stress (6 dynes/cm²) vs. high shear stress (16 dynes/cm²)(p<0.01). These data show that shear stress alters AQP1 abundance and subcellular distribution in vascular endothelial cells in vitro, thus supporting a role for AQP1 as an environmental sensor in HSV grafts.Grant Funding Source: Supported by the University of Dayton Research Council
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