OBJECTIVE: AGEs induce endothelial cell dysfunction in HUVECs, resulting in ROS production and triggering apoptosis. This study sought to identify miRNAs involved in AGE-induced @entity130 . METHODS: Microarray analysis to identify miRNAs altered with AGE stimulation was undertaken, and results were confirmed using real-time quantitative polymerase chain reaction. The interaction of miRNAs with the @entity3547 and @entity23759 genes was confirmed using luciferase assays, and their effects on expression were determined using Western blot analysis. The effects of AGEs and miRNAs on endothelial cell permeability were assessed. RESULTS: AGEs induced ROS production and apoptosis of HUVECs (p  <  0.05). AGE-induced @entity27164 and @entity18076 downregulation led to increased expression of their target genes, @entity3547 and ROCK, respectively. AGE-induced endothelial cell permeability and F-actin expression were significantly reduced with both @entity27164 and @entity18076 mimics (p  <  0.05). Furthermore, AGE-induced stress fiber formation was reduced in cells treated with @entity27164 mimics. CONCLUSION: @entity27164 and @entity18076 are suppressed in AGE-induced @entity130 , resulting in unregulated @entity3547 / @entity23759 signaling. Further studies are necessary to evaluate the therapeutic value of targeting miRNAs or their target genes for treatment of @entity455 .

Advanced glycation end products activate the miRNA/ @entity3547 / XXXX pathway in endothelial cells.

@entity455 :: ('MESH:D014652', 'Disease') :: ['vascular diseases'] @entity3547 :: ('387', 'Gene') :: ['RhoA'] @entity23759 :: ('9475', 'Gene') :: ['ROCK2'] @entity18076 :: ('406985', 'Gene') :: ['miR-200c'] @entity27164 :: ('406984', 'Gene') :: ['miR-200b'] @entity130 :: ('MESH:D014947', 'Disease') :: ['endothelial cell injury']
@entity23759 :: (9475,Gene) :: ['ROCK2']
