Gene perturbation in human arterial smooth muscle cells under treatments promoting synthetic or contractile phenotype

Smooth muscle cell (SMC) gene regulatory networks are thought to play a role in atherosclerosis, a disease characterized by alterations to SMC phenotype. Based on analysis of multiple bulk and single-cell RNA-Seq atherosclerosis data sets, FRZB and ALCAM were prioritized as candidate regulators of a disease-associated gene expression program in SMC-s. The current RNA-Seq experiment was devised to study the contribution of these genes to SMC transcriptional phenotype under different treatment conditions. RNA-Seq was used to profile gene expression in cultured human coronary artery smooth muscle cells. The cells were transduced with lentivirus overexpressing FRZB or transfected with siRNA silencing ALCAM to study the effect of these genes. Empty vector lentivirus and negative control siRNA were used as controls, respectively. Cells were treated with TGFbeta or cholesterol (or mock-treated for no treatment control) to induce atherosclerosis-relevant cellular phenotypes.