@entity621 accelerates calcification in cultured XXXX vascular smooth muscle cells.

@entity455 @entity621 @entity171 @entity5279 @entity4972 @entity620 @entity10210 @entity7305 @entity730 @entity692 @entity729 @entity731 @entity291
Calcification is a common feature of advanced @entity731 and is being reemphasized as a clinically significant element of @entity455 . However, the scarcity of in vitro models of @entity729 preclude studying its molecular and cellular mechanism. In the present study, we describe an in vitro calcification in which @entity730 can be induced by culturing @entity291 vascular smooth muscle cells (BVSMC) in the presence of @entity621 , @entity620 , and insulin in a manner analogous to in vitro mineralization by osteoblasts. Calcification was confirmed by von Kossa staining and 45Ca accumulation. Factor analysis revealed that @entity621 is the most important factor for this calcification process, suggesting that @entity4972 ( @entity4972 ) may be involved. As predicted, high levels of @entity4972 expression were detected by @entity4972 assay and Northern blot analysis. Functional significance of @entity4972 was confirmed by demonstrating that @entity7305 , a specific inhibitor of @entity4972 , inhibited BVSMC calcification in a dose-dependent manner. @entity171 such as @entity10210 and @entity5279 potently inhibited BVSMC calcification, suggesting that @entity692 formation may be involved. Importantly, expression of osteopontin mRNA was dramatically increased in calcified BVSMC compared with uncalcified control cells. These data suggest that @entity621 can induce @entity730 by an @entity4972 -dependent mechanism and that this in vitro calcification system is useful for analyzing the molecular and cellular mechanisms of @entity729 .
