{"title":"[FGF-2转染克隆高α -肌动蛋白水平的平滑肌细胞]。","authors":"C Allera, N Blaes","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":10555,"journal":{"name":"Comptes rendus de l'Academie des sciences. Serie III, Sciences de la vie","volume":"319 8","pages":"671-80"},"PeriodicalIF":0.0000,"publicationDate":"1996-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"[Smooth muscular cells with high alpha-actin level cloned by FGF-2 transfection].\",\"authors\":\"C Allera, N Blaes\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>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.</p>\",\"PeriodicalId\":10555,\"journal\":{\"name\":\"Comptes rendus de l'Academie des sciences. Serie III, Sciences de la vie\",\"volume\":\"319 8\",\"pages\":\"671-80\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1996-08-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Comptes rendus de l'Academie des sciences. Serie III, Sciences de la vie\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Comptes rendus de l'Academie des sciences. Serie III, Sciences de la vie","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
[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.