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首页> 外文期刊>Cellular Signalling >FGF-2 induces surfactant protein gene expression in foetal rat lung epithelial cells through a MAPK-independent pathway.
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FGF-2 induces surfactant protein gene expression in foetal rat lung epithelial cells through a MAPK-independent pathway.

机译：FGF-2通过不依赖MAPK的途径诱导胎鼠肺上皮细胞表面活性剂蛋白基因表达。

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Fibroblast growth factors (FGFs) play important roles in diverse aspects of animal development including mammalian lung epithelial cell proliferation, differentiation, and branching morphogenesis. We developed an in vitro lung epithelial cell culture system to study functions and mechanisms of FGFs in regulating growth and differentiation of primary foetal rat lung epithelial cells. In comparison with other growth factors such as IGF-I, EGF, and HGF, FGFs were the most potent mitogens in stimulating lung epithelial cell proliferation. In the presence of FGF-1, 2, or 7, the primary lung epithelial cells could be propagated for generations and grown for more than two mo in vitro. Among the three FGFs tested, FGF-7 showed the strongest stimulation in cell growth. FGF-2, on the other hand, is the most effective inducer of lung epithelial cell-specific surfactant protein gene expression (SP-A, -B, and -C). FGF-2 upregulated SP-C expression in a dose-dependent manner. More interestingly, the induction of surfactant protein gene expression by FGF-2 appeared to be independent of MAPK pathway, since the SP-C expression was not inhibited but rather augmented by MEK1 inhibitor which inhibited MAPK activation and cell proliferation. Similar effects were observed for the expressions of surfactant protein genes SP-A and SP-B. In contrast to MAPK, FGF-2-induced SP-C expression was partially inhibited by PI 3-kinase inhibitor wortmannin. These data suggest dynamic roles and complex signalling mechanisms of FGFs in regulating lung epithelial cell proliferation and differentiation. While a MAPK-dependent pathway is essential for all three FGFs to stimulate cell proliferation, a MAPK-independent pathway may be responsible for the FGF-2-induced surfactant protein gene expression. PI 3-kinase may play an important role in mediating FGF-2-induced lung epithelial cell differentiation during development.
机译：成纤维细胞生长因子（FGFs）在动物发育的各个方面都发挥着重要作用，包括哺乳动物肺上皮细胞的增殖，分化和分支形态发生。我们开发了体外肺上皮细胞培养系统，以研究FGF在调节原代胎鼠肺上皮细胞生长和分化中的功能和机制。与其他生长因子（例如IGF-1，EGF和HGF）相比，FGFs是刺激肺上皮细胞增殖最有效的促细胞分裂剂。在存在FGF-1、2或7的情况下，原代肺上皮细胞可以繁殖数代，并在体外生长超过两个月。在测试的三种FGF中，FGF-7在细胞生长中表现出最强的刺激作用。另一方面，FGF-2是肺上皮细胞特异性表面活性剂蛋白基因表达（SP-A，-B和-C）的最有效诱导剂。 FGF-2以剂量依赖性方式上调SP-C表达。更有趣的是，FGF-2对表面活性剂蛋白基因表达的诱导似乎与MAPK途径无关，因为SP-C的表达没有被抑制，而是被抑制MAPK活化和细胞增殖的MEK1抑制剂所增强。对于表面活性剂蛋白基因SP-A和SP-B的表达，观察到类似的效果。与MAPK相反，PI 3-激酶抑制剂渥曼青霉素可部分抑制FGF-2诱导的SP-C表达。这些数据表明FGF在调节肺上皮细胞增殖和分化中的动态作用和复杂的信号传导机制。尽管MAPK依赖性途径对于所有三种FGF刺激细胞增殖都是必不可少的，但MAPK依赖性途径可能是FGF-2诱导的表面活性剂蛋白基因表达的原因。在发育过程中，PI 3-激酶可能在介导FGF-2诱导的肺上皮细胞分化中起重要作用。

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