Transfection of miR-133a inhibitor significantly decreased intracellular miR-133a level (Figure 4A), and similar to what we found in the ischemic muscle, miR-133a antagonism in HUVECs under hyperglycemia and HSS conditions increased GCH1 protein expression (Figure 4B), tube formation (Figure 4C), NO (Figure 4D) and cGMP (Figure 4E), and decreased ROS level (Figure 4F). This evidence concerns the gene GCH1 and Hyperglycemia.