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Aims/Introduction  Diabetes mellitus is a major risk factor in the development of cardiovascular diseases ( CVD s). The presence of advanced glycation end‐products ( AGE s) promotes  CVD s by upregulating endothelial cell ( EC ) inflammatory and thrombotic responses, in a similar manner as disturbed shear stress. However, the combined effect of disturbed shear stress and  AGE s on  EC  function has yet to be determined. Our goal was to evaluate these effects on  EC  responses.    Materials and Methods   EC s were incubated with  AGE s for 5 days.  EC s were then subjected to physiological or pathological shear stress. Cell metabolic activity, surface expression of intercellular adhesion molecule‐1, thrombomodulin, connexin‐43 and caveolin‐1, and cytoskeleton organization were quantified.    Results  The results show that irreversibly glycated albumin and pathological shear stress increased  EC  metabolic activity, and upregulated and downregulated the  EC  surface expression of intercellular adhesion molecule‐1 and thrombomodulin, respectively. Expression of connexin‐43, caveolin‐1 and cytoskeletal organization was independent of shear stress; however, the presence of irreversibly glycated  AGE s markedly increased connexin‐43, and decreased caveolin‐1 expression and actin cytoskeletal connectivity.    Conclusions  Our data suggest that irreversibly glycated albumin and disturbed shear stress could promote  CVD  pathogenesis by enhancing  EC  inflammatory and thrombotic responses, and through the deterioration of the cytoskeletal organization.

journal of diabetes investigation

Combined effects of physiologically relevant disturbed wall shear stress and glycated albumin on endothelial cell functions associated with inflammation, thrombosis and cytoskeletal dynamics