Regulating the migration of vascular smooth muscle cells (VSMCs) is critical in tissue engineering and therapy of cardiovascular disease.
All compounds inhibited replication and all but fispemifene inhibited migration of vascular SMC and cells from cultured aortic explants in vitro.
We investigated the relationship between intracellular calcium ([Ca2+]i) and migration of vascular SMCs in response to platelet-derived growth factor (PDGF) and extracellular matrix (ECM) proteins.
The dedifferentiation, proliferation and migration of vascular smooth muscle cells (VSMCs) are essential in the progression of hypertension, atherosclerosis and intimal hyperplasia.
Apelin-13 induces proliferation and migration of vascular smooth muscle cells (VSMCs) as well as the upregulation of osteopontin (OPN) via the upregulation of Egr-1.
The abnormal proliferation and migration of vascular smooth muscle cells (SMCs) play an important role in the pathology of coronary artery atherosclerosis and restenosis following angioplasty.
Similarly, heparanase activity is implicated in neovascularization, inflammation and autoimmunity, involving migration of vascular endothelial cells and activated cells of the immune system [14], [15], [16].
Interestingly, we demonstrated here that MVL-PLA2 impairs adhesion and migration of vascular endothelial cell, as well as in vitro and in vivo angiogenesis.
Based on these data, it is clear that NOX1 and derived ROS products impede the migration of vascular smooth muscle and tumor cells.
VEGF is one of the most potent stimulators of angiogenesis by stimulating the proliferation and migration of vascular endothelial cells [30] [32].
Activation of the mitogen-activated protein kinase (MAPK) is known to be an important step in the migration of vascular smooth muscle cells [34], [35].
