FGF10 is required for cell proliferation and gland formation in the stomach epithelium of the chicken embryo
FGF10 is required for cell proliferation and gland formation in the stomach epithelium of the chicken embryo
复制标题
DOI：
10.1016/j.ydbio.2005.12.019
复制
发表时间：
2006-06-01
影响因子：
2.7
通讯作者：
Yasugi, Sadao
中科院分区：
文献类型：
--
作者：
Shin, Masahiro;Noji, Surnihare;Yasugi, Sadao
脊椎动物消化器官的发育涉及活跃的上皮-间充质相互作用。在鸡的腺胃中，上皮的形态发生和细胞分化是由其下层间充质分泌的诱导信号因子控制的。以前的研究表明，Fgf10在发育中的鸡室旁间充质中表达，而其受体存在于上皮细胞中。在我们目前的研究中，我们发现FGF10是一种早期间充质信号，与室旁上皮的发育过程密切相关。此外，病毒介导的Fgf10在OVO中过表达导致上皮结构的过度形态和上皮细胞数量的增加。相反，分泌的FGFR2b(SFGFR2b)(FGFR2b)是一种FGF10拮抗剂，它的过度表达阻止了卵子中腺上皮细胞的增殖和腺体的形成。这种增殖活性的下调随后被发现延缓了腺体的形成，也延缓了上皮的分化。这些结果表明，在发育中的鸡胚胎中，FGF10信号是由FGFR1b和/或FGFR2b介导的，是上皮细胞增殖和腺体形成所必需的。(C)2005 Elsevier Inc.保留所有权利。
The development of digestive organs in vertebrates involves active epithelial-mesenchymal interactions. In the chicken proventriculus (glandular stomach), the morphogenesis and cytodifferentiation of the epithelium are controlled by the inductive signaling factors that are secreted from the underlying mesenchyme. Previous studies have shown that Fgf10 is expressed in the developing chicken proventricular mesenchyme, whereas its receptors are present in the epithelium. In our present study, we show that FGF10 is an early mesenchymal signal that is critically associated with the developmental processes in the proventricular epithelium. Furthermore, virus-mediated Fgf10 overexpression in ovo results in a hypermorphic epithelial structure and an increase in epithelial cell number. In contrast, the overexpression of a secreted FGFR2b (sFGFR2b), an FGF10 antagonist, blocks cell proliferation and gland formation in the proventricular epithelium in ovo. This downregulation of proliferative activity was subsequently found to retard gland formation and also to delay differentiation of the epithelium. These results demonstrate that FGF10 signaling, mediated by FGFR1b and/or FGFR2b, is required for proliferation and gland formation in the epithelium in the developing chick embryo. (c) 2005 Elsevier Inc. All rights reserved.