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首页> 外文期刊>The FEBS journal >Intracellular trafficking of endogenous fibroblast growth factor-2
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Intracellular trafficking of endogenous fibroblast growth factor-2

机译：内源性成纤维细胞生长因子2的细胞内运输

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We have previously reported how the release of fibroblast growth factor-2 (FGF-2) is mediated by shed vesicles. In the present study, we address the question of how newly synthesized FGF-2 is targeted to the budding vesicles. Considering that in vitro cultured Sk-Hep1 hepatocarcinoma cells release FGF-2 and shed membrane vesicles only when cultured in the presence of serum, we added serum to starved cells and monitored intracellular movements of the growth factor. FGF-2 was targeted both to the cell periphery and to the nucleus and nucleolus. Movements toward the cell periphery were not influenced by drugs affecting microtubules, but were inhibited by cytocalasin B. Involvement of actin in FGF-2 trafficking toward the cell periphery was supported by coimmunoprecipitation and immune localization experiments. Colocalization of FGF-2 granules moving to the cell periphery and FM4-64-labelled intracellular lipids were not observed. Ouabain and methylamine, two inhibitors of FGF-2 release, were analyzed for their effects on FGF-2 intracellular localization and on vesicle shedding. Ouabain inhibited FGF-2 movements toward the cell periphery. The FGF-2 content of shed vesicles was therefore reduced. Methylamine inhibited vesicle shedding; in its presence, FGF-2 clustered at the cell periphery, but the rate of its release decreased. FGF-2 targeting to the nucleus and nucleolus was not affected by cytocalasin B, whereas it was inhibited by drugs that modify microtubule dynamics. Neither ouabain, nor methylamine interfered with FGF-2 translocation to the nucleus and nucleolus. FGF-2 targeting to the budding vesicles and to the nucleus and nucleolus is therefore mediated by fundamentally different mechanisms.
机译：我们以前曾报道过脱落的囊泡如何介导成纤维细胞生长因子2（FGF-2）的释放。在本研究中，我们解决了新合成的FGF-2如何靶向发芽囊泡的问题。考虑到体外培养的Sk-Hep1肝癌细胞仅在有血清的情况下培养时才释放FGF-2并脱落膜小泡，我们将血清添加到饥饿的细胞中并监测生长因子的细胞内运动。 FGF-2既靶向细胞周边，又靶向细胞核和核仁。向细胞外围的移动不受影响微管的药物的影响，但受到细胞松弛素B的抑制。肌动蛋白参与FGF-2向细胞外围的运输受到共免疫沉淀和免疫定位实验的支持。没有观察到移动到细胞外围的FGF-2颗粒和FM4-64标记的细胞内脂质的共定位。分析了两种FGF-2释放抑制剂瓦巴因和甲胺对FGF-2细胞内定位和囊泡脱落的影响。哇巴因抑制FGF-2向细胞周围的运动。因此，脱落的囊泡的FGF-2含量降低。甲胺抑制囊泡脱落;在其存在下，FGF-2聚集在细胞外围，但其释放速率下降。 FGF-2靶向细胞核和核仁不受细胞松弛素B的影响，而被修饰微管动力学的药物抑制。哇巴因和甲胺均不干扰FGF-2转运至细胞核和核仁。因此，通过根本不同的机制介导针对发芽囊泡以及细胞核和核仁的FGF-2。

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