[FGF-2转染克隆高α -肌动蛋白水平的平滑肌细胞]。

C Allera, N Blaes
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引用次数: 0

摘要

众所周知,成纤维细胞生长因子2 (FGF-2)在动脉平滑肌细胞(SMC)中的作用是调节增殖和迁移。我们在这里通过感觉cDNA转染显示,内源性FGF-2表达控制SMC克隆的α -肌动蛋白水平。所有α -肌动蛋白高表达克隆均转染了FGF-2。与亲本培养物相比,携带缺失载体的对照克隆表现出弱表达和肌动蛋白聚合的改变。在FGF-2转染的克隆中,α -肌动蛋白的表达是异质性的,表达水平高低不一。这些观察结果是使用正常大鼠SMC或来自转化细胞系的SMC获得的。它们表明内源性FGF-2在动脉SMC分化中的作用。我们的研究结果表明,FGF-2可能通过允许已经分化的细胞克隆生长或调节α -肌动蛋白的表达或稳定性来起作用。为动脉壁基因治疗开辟了新的前景。
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[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.

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