Vascular smooth muscle cells (VSMC) take a central role in the onset and progression of many cardiovascular diseases, from atherosclerosis to vascular injury or restenosis, where their migration and matrix degradation function is deregulated. While generally responsible for maintaining the contractile tonus of the vessel walls and regulating the blood flow, VSMCs lose their contractility in response to the vascular injury, or during the disease progression and switch to a migratory phenotype. Recent data indicates that the switch is significantly enabled by the formation of podosomes, integrin-rich adhesive and mechanically protrusive structures at the matrix interface of the plasma membrane.
Matrix rigidity as well as blood pressure can promote the formation of podosomes. However, the details of the regulation of podosome mechanosensing are still elusive.
Here we study how podosomes interact with their microenvironment and how this determines the cell phenotype, to gain a greater understanding of the role of VSMCs in cardiovascular diseases.