Abstrakt
Vascular smooth muscle cells (VSMCs) play important roles not only in the physiological functions of the blood vessels, such as vasoconstriction, vasodilatation and extracellular matrix production, but also in the pathogenesis of vascular diseases, particularly atherosclerosis and hypertension. VSMCs are mostly of mesodermal origin, although some are of neuroectodermal origin, for example, VSMCs present in the aorta and in blood vessels arising from the aortic arch.
VSMCs of neuroectodermal origin are implicated in defects of cardiovascular morphogenesis, such as bicuspid aortic valve, coarctation of the aorta, patent ductus arteriosus and tetralogy of Fallot. The origin, location in the vascular tree, gender, species, strain and age influence the phenotype of VSMCs and their propensity to migration and growth.
In a healthy adult organism, VSMCs have a quiescent and differentiated contractile phenotype characterized by early markers (e.g., SM α-actin, SM22-α), intermediate markers (h-caldesmon, calponin) and late markers (SM myosins, smoothelin) of VSMC differentiation. However, after blood vessel injury, surgery or explantation in vitro, VSMCs undergo a phenotypic modulation to synthetic phenotype, which endows them with high activity in migration, growth and proteosynthesis.
These features can lead to stenosis or to obliteration of the vascular lumen and impaired blood supply to various tissues and organs.