The most common cause for chronic term (> 30 days) failure of vascular bypass grafts is the rapid growth of underlying tissues within arteries called intimal hyperplasia (EH) [1]. IH has been found to primarily exist in low wall shear stress regions within distal anastomoses [2]; however, the exact mechanism by which shear stress induces IH has not been ascertained. We hypothesize that endothelial lining permeability is induced by wall shear stress during tissue reorganization such as occurs within vascular bypass constructs. Occludin is an adhesion protein that is actively involved in endothelial cell (EC) tight junctions, and thus, may effect EC layer permeability. To date, no studies have been conducted to determine the effect of wall shear stress on this adhesion protein. Therefore, the purpose of this study is to evaluate the role of wall shear stress upon the expression of occludin within cultured endothelial cells.

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