(A) Elk1 has previously been validated as a miR-143/145-repressed gene. Elk1-3’UTR-Luciferase construct was transfected into wt and c-myblx/lx carotid artery VSMC. Luciferase activity was assayed on PHERASTAR and found to be augmented in c-myblx/lx VSMC, which have known reductions in c-Myb expression (p<0.01**). (B) Time course analysis of c-Myb and Elk-1 expression. After serum starvation and cell cycle arrest, c-Myb levels are diminished. Following addition of 10% fetal bovine serum, c-Myb expression peaks at 12 h. As c-Myb expression level rise, Elk-1 expression levels decrease and are undetectable at 12 h. Note that c-Myb expression is not detectable in c-myblx/lx VSMC released from serum starvation, and Elk-1 expression remains stable. (C) miR-143 mediates c-Myb repression of Elk1. The miR-143 antagomir augments Elk-1 protein expression in wt cells that express c-Myb, while the mimic abrogates protein expression in c-myblx/lx VSMC.