Modeling cell migration with

Modeling cell migration with persistent random walk models... 

The effect of biomaterial scaffolds on NSCs has been investigated following TBl. Tate et al. (2002) transplanted mouse NSCs with or without fibronectin/collagen 1 (Fn) scaffolds 1 week after TBl in a mouse model. Cells transplanted with the Fn scaffolds showed increased survival and migration to the hippocampus compared to cells alone. They also examined using laminin scaffolds in a second study that both scaffolds improved cell survival at 8 weeks and the laminin scaffolds showed improved cognitive function at 5 weeks (Tate et al. 2009). These studies demonstrate that stem cell transplantation may hold a potential as a treatment for TBl and that biomaterials scaffolds may improve cell survival and functional outcomes. 

The calcification of atherosclerotic plaques may be induced by osteopontin expression, since osteopontin is a protein with a well-characterized role in bone formation and calcification. Vascular smooth muscle cell migration on osteopontin is dq endent on the integrin av 33 and antagonists of av 33 prevent both smooth muscle cell migration and restenosis in some animal model [8]. 

The chemotaxis of mononuclear leukocytes and the migration, growth, and activation of the multiple cell types within atherosclerotic lesions are critical for the chronic inflammatory and fibroproliferative response in atherosclerosis (Ml). Chemokine-mediated attraction of leukocytes to tissues has been shown in atherosclerotic lesions (G8). Studies using knockout and transgenic murine models indicated that chemokine receptor/ligand interactions are crucial in the development of atherosclerosis (P6). Moreover, chemokines may also interfere with smooth muscle cell migration and growth, and platelet activation and other well-defined features of the atherosclerotic process (A2). 

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