Using cultured VSMCs, we found that Ang II increased cellular OPN protein expression 4?h after treatment by 420?¡À?54 % (p?<?0.03) in a translation dependent manner. Sequence analysis revealed a putative binding site for mir181a and raised the possibility that miR181a is a potential regulatory mechanism for OPN expression. We demonstrated that Ang II decreased miR181a expression by 52?¡À?7 % (p?<?0 .0001) and overexpressing miR181a inhibited Ang II induced increases in OPN protein expression by 69?¡À?9 % (p?<?0.05). Furthermore, we demonstrated that miR181a is functionally important in that overexpression of miR181a inhibited VSMCs adhesion to collagen in response to Ang II as compared to controls by 36?¡À?4 % . (p?<?0.05)
These results demonstrate that miR181a regulates OPN expression and that altering miR181a expression may be a novel therapeutic approach to modulate OPN protein expression.