[Smooth muscular cells with high alpha-actin level cloned by FGF-2 transfection].
Regulation of proliferation and migration are well known roles of fibroblast growth factor 2 (FGF-2) for arterial smooth muscle cells (SMC). We show here, by sense cDNA transfection that endogenous FGF-2 expression controls alpha-actin level in SMC clones. All the high alpha-actin expressing clones were FGF-2 transfected. Control clones carrying a deleted vector showed a weak expression and an altered actin polymerisation compared to the parental cultures. Among FGF-2 transfected clones, alpha-actin expression was heterogenous with diversely high levels. These observations were obtained using normal rat SMC or SMC from a transformed cell line. They indicate a role for endogenous FGF-2 in arterial SMC differentiation. Our results suggest that FGF-2 might act either by permissing clonal growth of already differentiated cells or by regulating expression or stability of alpha-actin. They open new perspective for gene therapy of the arterial wall.
Allera
C
C
INSERM U. 397, Institut Louis-Bugnard, CHU Rangueil, Toulouse, France.
Blaes
N
N
D000199:Actins / Q000032:analysis*; D000818:Animals; D002454:Cell Differentiation; D002999:Clone Cells / Q000737:chemistry; D016222:Fibroblast Growth Factor 2 / Q000235:genetics*; D015870:Gene Expression; D005822:Genetic Vectors; D009131:Muscle, Smooth, Vascular / Q000737:chemistry* / Q000166:cytology; D051381:Rats; D017208:Rats, Wistar; D014162:Transfection; D019076:Transgenes
D000199:Actins; D016222:Fibroblast Growth Factor 2
Cellules musculaires lisses à taux d'alpha-actine élevé clonées par transfection FGF-2.