XXXX inhibits cell proliferation by involving transforming growth factor-beta.

@entity137 @entity301 @entity5 @entity117 @entity1810 @entity35 @entity1281
BACKGROUND: @entity117 ( @entity1281 ) inhibits cell proliferation. This may be mediated by transforming growth factor-beta ( @entity1810 ). @entity1810 directly stops cell proliferation, restrains cells in G(0), and inhibits the uptake of platelet-derived growth factor and insulin-like growth factor. These effects are identical to those observed with @entity1281 treatment. METHODS AND RESULTS: We cultured @entity35 thoracic aorta vascular smooth muscle cells and measured @entity137 , cell proliferation, cell cycle, transcription of @entity1810 , and concentration of @entity1810 in supernatant medium. @entity1281 dose-dependently restrained cells in G(0) phase with no cytotoxic effect and inhibited cell proliferation by 30.86%. Anti- @entity1810 reversed this inhibition by 30.21%. However, @entity1281 treatment decreased @entity1810 transcription and had no significant effect on @entity1810 concentration. CONCLUSIONS: @entity1810 seems to play an important role in @entity1281 -mediated inhibition of cell proliferation. Therefore, treatment with @entity1281 prevents @entity301 not only by means of its antiplatelet properties but also by an important inhibition of plaque growth. This relationship between @entity1281 and @entity1810 explains many other effects, such as @entity5 chemoprevention, immunomodulation, and wound healing. The aim of this study was to demonstrate this link.
