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• _4 value "Surprisingly, despite the lack of severing activity, capG overexpression also increased fibroblast motility [42]. Gelsolin has also been shown to regulate hematopoietic stem cell motility. Lin-Sca+Kit+ and Lin-Sca+Kit-, are two hematopoietic stem cell populations which show different basal and induced motility capacity. Indeed, they exhibit differential cell motility in response to stromal derived factor 1 (SDF-1), a chemokine influencing cell motility through phosphatidylinositol signaling. Lin-Sca+Kit+ cells, which are more primitive than Lin-Sca+Kit- cells, exhibit a lower response in terms of cell motility, although the activation of the phosphatidylinositol pathway was activated at the same level in the two populations. Proteomics analysis documented a lower expression of gelsolin and adseverin in Lin-Sca+Kit+ than in Lin-Sca+Kit-, providing an explanation for this differential response to SDF-1 [43]. CapG, which lacks severing activity, has also been shown to be involved in regulation of cellular motility in fibroblastic cells [42]. More recently, we were able to demonstrate that capG is also an important regulator of motility function in endothelial cells [29]. Endothelial cells are able to discriminate between different combinations of mechanical forces. In vivo, this capability results in a focalization of vascular areas subjected to atherosclerotic plaque development [44-46]. Indeed, plaques develop at bifurcations and curvatures which are exposed to a particular pattern of blood flow, with a low mean shear stress value and cyclic reversal of flow direction, which is in contrast with the unidirectional pattern of flow characterizing vascular areas protected against plaque development. In response to a plaque-free hemodynamic environment, capG expression and consequently endothelial motility are increased [29], resulting in a faster wound healing process [47], as compared to endothelial cells exposed to plaque-prone conditions. In vivo evidence for gelsolin involvement in cell motility was provided by gelsolin null mice (Gsn-/-), in which motility of osteoclasts was decreased [48]. In these mice, osteoclasts were unable to form cell adhesion structures (podosomes), and therefore their basal as well as their osteopontin- induced motility was affected. Analysis of these mice identified an additional role of gelsolin in the regulation of neuronal growth, cone formation and retraction [49]. Neuronal growth cones are highly motile structures from which lamellipodia and filopodia form and retract. Formation of these structures is a Ca2+-controlled process dependent on actin cytoskeleton remodeling. In Gsn-/- mice, only retraction processes appeared to be delayed, as compared to wild-type mice, suggesting that retraction is solely dependent on the presence of gelsolin," provenance.
• _4 wasQuotedFrom 15526166 provenance.