Integrin α7β1 COMPels smooth muscle cells to maintain their quiescence

cartilage oligomeric matrix protein; extracellular matrix; vascular injury Arterial smooth muscle cells (SMCs) normally reside in the arterial wall in a differentiated contractile state. Following injury, such as that caused by angioplasty or stenting, or in more chronic conditions, such as atherosclerosis, some SMCs in the arterial wall convert to a less differentiated state, often termed de-differentiated, synthetic, or proliferative state.1 These de-differentiated or synthetic SMCs gain the ability to respond to growth factors, and to migrate and proliferate. At the same time, they lose several cytoskeletal markers of differentiation and most likely their ability to respond to contractile stimuli and to contribute to vessel contraction. It has long been known that there is an inverse correlation between SMC proliferation and their expression of cytoskeletal markers of differentiation.2 Understanding of the factors regulating SMC differentiation is important, because maintaining SMC differentiation in conditions normally associated with increased SMC de-differentiation would most likely prevent restenosis following angioplasty and development of irreversible atherosclerotic lesions characterized by SMC proliferation and migration. What are the extracellular cues that determine the differentiation state of SMCs? It has bee