GAS6 Induces Axl-mediated Chemotaxis of Vascular Smooth Muscle Cells

摘要: Atherosclerosis and arterial restenosis are disease processes involving the accumulation of vascular smooth muscle cells following injury. Key events leading to these migration proliferation cells. Here, we demonstrate that GAS6, encoded by growth arrest-specific gene 6, induces a directed (chemotaxis) both rat human primary while showing only marginal mitogenic potential in GAS6 stimulation Axl autophosphorylation cells, indicating specific GAS6-Axl interactions may be associated with GAS6-directed chemotaxis. To test this hypothesis, overexpressing were generated transfer assessed for their ability migrate along gradient. These overexpressors exhibited 2-5-fold increased sensitivity GAS6-induced Furthermore, expressing kinase dead mutant or exposure soluble extracellular domain showed attenuated migration. Taken together, results suggest is novel chemoattractant Axl-mediated The separation mitogenesis from provided study enhance molecular dissection cell damage.