Low shear stress induces endothelial cell apoptosis and monocyte adhesion by upregulating PECAM-1 expression.

Low shear stress serves an important role in the initiation and progression of atherosclerotic lesions, with an impact on progression, but its detailed mechanisms are. not yet fully known. The present study aimed to investigate endothelial cell (EC) apoptosis, as well as monocyte adhesion induced by low shear stress and the potential underlying mechanisms. The expression of platelet endothelial cell adhesion molecule-1 (PECA M-1) was demonstrated to be enhanced in human umbilical vascular EC s with a trend that was associated with time when stimulated by low shear stress compared with unstimulated cells. EC apoptosis was increased under low shear stress compared with unstimulated cells, and knockdown of PECA M-1 inhibited this process. Furthermore, downregulation of PECA M-1 reduced monocyte adhesion induced by low shear stress compared with that in the negative control cells. Mechanistically, PECA M-1 small interfering RNA transfection increased Akt and forkhead box O1 phosphorylation under low shear stress conditions compared with that in the negative control cells. Collectively, the findings of the present study revealed that low shear stress induced EC apoptosis and monocyte adhesion by upregulating PECA M-1 expression, which suggested that PECA M-1 may be a potential therapeutic target for atherosclerosis. [ABSTRACT FROM AUTHOR]