Sustained orbital shear stress stimulates smooth muscle cell proliferation via the extracellular signal-regulated protein kinase 1/2 pathway

After an endothelial-denuding injury such as angioplasty, SMCs are directly exposed to hemodynamic forces such as shear stress. Although the exact nature of the shear stress to which the SMCs are exposed in vivo has not yet been defined, the shear-stress forces are likely to be complicated or even turbulent. The orbital shaker produces shear stress that directly stimulates SMC proliferation, suggesting its usefulness as an in vitro model. Because orbital shear-stress-induced SMC proliferation and phenotype modulation is at least partly mediated by the ERK1/2 pathway, shear-stress-stimulated SMC proliferation after vascular injury may be mediated by a pathway amenable to pharmacologic manipulation.