Understanding differences in gene expression that increase risk for pulmonary arterial hypertension (PAH) is essential to understanding the molecular basis for disease. Previous studies on patient samples were limited by either end-stage disease effects or by use of non-adherent cells which are not ideal to model vascular cells in vivo. These studies addressed the hypothesis that pathological processes associated with PAH may be identified via a genetic signature common across multiple cell types. Expression array experiments were initially conducted analyzing cell types at different stages of vascular differentiation (mesenchymal stromal and endothelial) derived from PAH patient specific induced pluripotent stem cells (iPS cells). Molecular pathways which were altered in the PAH cell lines were then compared to fibroblasts from 21 patients, including both idiopathic and heritable PAH. Wnt was identified as a target pathway and validated in vitro using primary patient mesenchymal and endothelial cells. Taken together, our data suggest that the molecular lesions that cause PAH are present in all cell types evaluated regardless of origin and that stimulation of the Wnt signaling pathway was a common molecular defect in both heritable and idiopathic PAH.