FGF-2 TRANSFECTION INDUCES HIGH ALPHA-ACT IN LEVEL IN ARTERIAL SMOOTH-MUSCLE CELL CLONES

Regulation of proliferation and migration are well known roles of fibr oblast growth factor 2 (FGF-2) for arterial smooth muscle cells (SMC). We show here, by sense cDNA transfection that endogenous FGF-2 expres sion controls alpha-actin level in SMC clones. All the high alpha-acti n expressing clones were FGF-2 transfected. Central clones carrying a deleted vector showed a weak expression and an altered actin polymeris ation compared to the parental cultures. Among FGF-2 transfected clone s, alpha-actin expression was heterogenous with diversely high levels. These observations were obtained using normal rat SMC or SMC from a t ransformed cell line. They indicate a role for endogenous FGF-2 in art erial SMC differentiation. Our results suggest that FGF-2 might act ei ther by permissing clonal growth of already differentiated cells or by regulating expression or stability of alpha-actin. They open new pers pective for therapy of the arterial wall.