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首页> 外文期刊>Journal of Cellular Physiology >Upregulation of molecular motor-encoding genes during hepatocyte growth factor- and epidermal growth factor-induced cell motility.
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Upregulation of molecular motor-encoding genes during hepatocyte growth factor- and epidermal growth factor-induced cell motility.

机译：Upregulation分子motor-encoding基因在肝细胞生长因子和表皮生长因素细胞的能动性。

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Hepatocyte growth factor (HGF) and epidermal growth factor (EGF) are known to stimulate the locomotion of epithelial cells in culture. However, the molecular mechanisms which mediate these important changes are poorly understood. Here we have determined the effects of HGF and EGF on hepatocyte morphology, cytoskeletal organization, and the expression of molecular motor-encoding genes. Primary cultures of hepatocytes were treated with 10 ng/ml of HGF or EGF and observed with phase and fluorescence microscopy at 10, 24, and 48 h after treatment. We found that, over time, treated cells spread and became elongated after 24 h of treatment while forming long processes with dramatic alterations in the microtubule and actin cytoskeletons by 48 h. Quantitative Northern blot analysis was performed to measure expression of cytoskeletal-(beta-actin, alpha-tubulin) and molecular motor-(dynein, kinesin, and myosin I alpha and II) encoding genes which may contribute to this change in form. We observed the highest increase in levels of expression for myosin II (3.3-fold), kinesin (2.7-fold), myosin I alpha (2.2-fold), and alpha-tubulin (1.9-fold) after only 2 h of treatment with HGF. In contrast, EGF upregulated the expression of myosin I alpha (2.4-fold), kinesin (1.5-fold), and dynein (1.5-fold) at 10 h. The expression of the beta-actin gene remained constant in HGF-treated cells, while EGF induced a slight upregulation after 10 h of treatment. These results show for the first time that a selective upregulation of molecular motor-encoding genes correlates with alterations in cell shape and motility induced by HGF and EGF.
机译：肝细胞生长因子(HGF)和表皮生长因子(EGF)是已知的刺激上皮细胞的运动文化。然而,调节的分子机制这些重要的变化知之甚少。我们已经确定HGF和的影响表皮生长因子在肝细胞形态、细胞骨架组织和分子的表达motor-encoding基因。肝细胞治疗胶质瘤或10 ng / mlEGF和阶段和荧光观察显微镜在10、24和48 h后治疗。我们发现,随着时间的推移,治疗细胞扩散并成为延长治疗24小时后而形成长流程与戏剧性改变微管和肌动蛋白骨骼由48 h。定量北部污点分析了测量的表达细胞骨架(beta-actin alpha-tubulin)和分子马达(动力蛋白,驱动蛋白和肌凝蛋白α和II)编码基因可能的贡献这种形式的变化。增加肌凝蛋白水平的表达(3.3倍),驱动蛋白(2.7倍),α肌球蛋白(2.2倍),alpha-tubulin(1.9倍)只有2 h与胶质瘤的治疗。调节α肌凝蛋白的表达(2.4倍),驱动蛋白(1.5倍),和动力蛋白(1.5倍)10 h的表达beta-actin HGF-treated基因保持不变细胞,而EGF诱导略微upregulation10 h后的治疗。第一次的选择性upregulation与分子motor-encoding基因引起的变化在细胞形状和能动性HGF和EGF。

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