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首页> 外文期刊>The international journal of developmental biology >Interplay between FGF10 and Notch signalling is required for the self-renewal of pancreatic progenitors
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Interplay between FGF10 and Notch signalling is required for the self-renewal of pancreatic progenitors

机译：胰腺祖细胞的自我更新需要FGF10和Notch信号之间的相互作用

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摘要

Recent studies have shown that persistent expression of FGF10 in the developing pancreas of transgenic mice results in enhanced and prolonged proliferation of pancreatic progenitors, pancreatic hyperplasia and impaired pancreatic differentiation. These studies have also suggested that FGF10 prevents the differentiation of pancreatic progenitors by maintaining persistent Notch signalling. Here, we provide experimental evidence sustaining the capacity of FGF10 to induce the proliferation of pancreatic precursors, while preventing their differentiation. Using explant cultures of E10.5 isolated dorsal pancreatic epithelium, we found that FGF10 maintained Notch activation and induced the expansion of pancreatic precursors while blocking their differentiation. In addition, by using a gamma-secretase inhibitor, we were able to down-regulate the expression of Hes1, a target gene of the Notch pathway in explant cultures of pancreatic epithelium treated with FGF10. In such explants, the effect of FGF10 on the proliferation and maintenance of pancreatic progenitors was suppressed. These results demonstrate that activation of the Notch pathway is required as a downstream mediator of FGF10 signalling in pancreatic precursor cells.
机译：最近的研究表明，FGF10在转基因小鼠的胰腺中持续表达会导致胰腺祖细胞增殖增强和延长，胰腺增生和胰腺分化受损。这些研究还表明，FGF10通过维持持续的Notch信号传导来阻止胰腺祖细胞的分化。在这里，我们提供实验证据，维持FGF10诱导胰腺前体增殖，同时防止其分化的能力。使用E10.5分离的背胰上皮的外植体培养物，我们发现FGF10维持Notch活化并诱导胰腺前体的扩增，同时阻止其分化。此外，通过使用γ-分泌酶抑制剂，我们能够下调在用FGF10处理的胰腺上皮的外植体培养物中Notch通路的靶基因Hes1的表达。在这些外植体中，FGF10对胰腺祖细胞增殖和维持的作用被抑制。这些结果表明，Notch途径的激活是胰腺前体细胞中FGF10信号传导的下游介质所必需的。

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