An atherosclerotic gene expression program.

Tcf21 drives biologically significant components in human disease. We studied total gene expression in cells genetically engineered to over-express Tcf21 in human coronary artery smooth muscle cells as a model for understanding component gene expression in human disease at the cellular level at the scale of the whole transcriptome. Tcf21 activated expression of the clotting related gene Tfpi2 and the damage associated factor Plau. Coronary artery smooth muscle cells over-expressing Tcf21 activated chemokines Ccl7 and Ccl11. Tcf21 induced expression of matrix metalloproteinase Mmp1 and clotting factor F2rl3. Tcf21 activated Cd82 and silenced Cd14 in cells of the heart. Tcf21 ectopic expression drove induction of Vipr1 and Pgf.