Project description:The mechanisms by which oscillatory shear (OS) induces, while high laminar shear stress (LS) prevents, atherosclerosis are still unclear. Here, we examined the hypothesis that OS induces inflammatory response, a critical atherogenic event, in endothelial cells by a miRNA-dependent mechanism. In particular, miR-663 mediated OS-induced inflammation through monocyte adhesion to endothelial cells. The potential targets of miR-663 were examined by knockdown of miR-663 and then the gene expression profiles were determined under shear stress conditions.
Project description:The mechanisms by which oscillatory shear (OS) induces, while high laminar shear stress (LS) prevents, atherosclerosis are still unclear. Here, we examined the hypothesis that OS induces inflammatory response, a critical atherogenic event, in endothelial cells by a miRNA-dependent mechanism. In particular, miR-663 mediated OS-induced inflammation through monocyte adhesion to endothelial cells. The potential targets of miR-663 were examined by knockdown of miR-663 and then the gene expression profiles were determined under shear stress conditions. To determine the potential targets of miR-663, HUVEC were transfected either with miR-663-LNA (inhibitor of miR-663) or control-LNA and then subjected to OS or LS for 24hr. Total RNA were collected from these four groups and microarray studies (Illumina HumanHT-12 v3 beadchip) were performed.