Department of Biochemistry and Biophysics, Programs in Developmental Biology, Genetics and Human Genetics, the Liver Center, Institute for Regeneration Medicine and Diabetes Center, University of California, San Francisco, CA 94158, USA.
Proc Natl Acad Sci U S A. 2010 Jan 19;107(3):1142-7. doi: 10.1073/pnas.0910205107. Epub 2009 Dec 29.
Bmp signaling has been shown to regulate early aspects of pancreas development, but its role in endocrine, and especially beta-cell, differentiation remains unclear. Taking advantage of the ability in zebrafish embryos to cell-autonomously modulate Bmp signaling in single cells, we examined how Bmp signaling regulates the ability of individual endodermal cells to differentiate into beta-cells. We find that specific temporal windows of Bmp signaling prevent beta-cell differentiation. Thus, future dorsal bud-derived beta-cells are sensitive to Bmp signaling specifically during gastrulation and early somitogenesis stages. In contrast, ventral pancreatic cells, which require an early Bmp signal to form, do not produce beta-cells when exposed to Bmp signaling at 50 hpf, a stage when the ventral bud-derived extrapancreatic duct is the main source of new endocrine cells. Importantly, inhibiting Bmp signaling within endodermal cells via genetic means increased the number of beta-cells, at early and late stages. Moreover, inhibition of Bmp signaling in the late stage embryo using dorsomorphin, a chemical inhibitor of Bmp receptors, significantly increased beta-cell neogenesis near the extrapancreatic duct, demonstrating the feasibility of pharmacological approaches to increase beta-cell numbers. Our in vivo single-cell analyses show that whereas Bmp signaling is necessary initially for formation of the ventral pancreas, differentiating endodermal cells need to be protected from exposure to Bmps during specific stages to permit beta-cell differentiation. These results provide important unique insight into the intercellular signaling environment necessary for in vivo and in vitro generation of beta-cells.
Bmp 信号已被证明能调节胰腺发育的早期阶段,但它在内分泌,特别是β细胞分化中的作用仍不清楚。利用斑马鱼胚胎中单个细胞自主调节 Bmp 信号的能力,我们研究了 Bmp 信号如何调节单个内胚层细胞分化为β细胞的能力。我们发现 Bmp 信号的特定时间窗口可阻止β细胞分化。因此,未来来自背侧芽的β细胞对 Bmp 信号的敏感性在原肠胚和早期体节形成阶段特异性增强。相比之下,需要早期 Bmp 信号形成的腹侧胰腺细胞在 50 hpf 时暴露于 Bmp 信号下不会产生β细胞,此时腹侧芽衍生的胰外导管是新内分泌细胞的主要来源。重要的是,通过遗传手段抑制内胚层细胞内的 Bmp 信号会增加β细胞的数量,无论是在早期还是晚期。此外,在晚期胚胎中使用 Dorsomorphin(一种 Bmp 受体的化学抑制剂)抑制 Bmp 信号,在胰外导管附近显著增加β细胞的新生,证明了使用药理学方法增加β细胞数量的可行性。我们的体内单细胞分析表明,虽然 Bmp 信号最初对于形成腹侧胰腺是必需的,但分化的内胚层细胞需要在特定阶段免受 Bmps 的暴露,以允许β细胞分化。这些结果为体内和体外生成β细胞所需的细胞间信号环境提供了重要的独特见解。