As shown by our previous results, biomechanical stretch is sufficient to control the switch from the
contractile to the synthetic smooth muscle cell (SMC) phenotype which is a prerequisite for venous and
arterial remodeling processes. With RGS5, NFAT-5 and AP-1, we identified a G-protein signalingregulating
protein and two transcription factors that control specific properties of contractile/synthetic
SMCs exposed to an increase in wall stress (WS) or stretch. This proposal is thus aimed at investigating
the functional properties and mechanisms regulating the activity of these molecules in venous and
arterial SMCs during chronic and acute vascular diseases.