近日，来自丹麦哥本哈根大学和哈格多恩研究所干细胞中心（DanStem）的科学家们在控制身体胰岛素产生的信号路径上有了新的突破。研究人员将干细胞转化产生胰岛素的β细胞，β细胞可以植入到需要它们的病人体内。相关研究论文发表在新一期PNAS杂志上。
胰岛素是由胰腺中的β细胞产生的一种激素。如果这些β细胞有缺陷的话，机体会发展有糖尿病。糖尿病患者往往通过每天注射胰岛素来维持血糖，胰岛素是至关重要的。科学家们希望，在不那么遥远的未来，这项研究发现将有可能更有效地治疗糖尿病，为糖尿病患者提供新的运作良好的β细胞，以防止继发性疾病如心脏病、失明、神经及肾脏并发症的发生。
Palle Serup教授解释说：“为了让干细胞发展成胰岛素生产β细胞，有必要知道在胎儿的发育过程中是什么信号机制控制并创造β细胞。我们新的研究成果能”。
教授Serup表示：当我们知道具体信号途径时，我们可以在试管中进行复制，从而及时将干细胞转换成β细胞。
控制干细胞发展成β细胞的信号途径的第一步老早就被科学家所知。该研究发现Notch信号通路培育的干细胞更有效地转换成产生胰岛素的β细胞非常重要。这项新的研究为下一步的细胞的发展以及细胞之间沟通的信号铺平道路， 这还是个没有被广泛认知的领域知识。（生物谷：Bioon.com）
doi:10.1073/pnas.1203605109
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Mind bomb 1 is required for pancreatic β-cell formation
Signe Horna, Sune Kobberupa, Mark Kalisza, Tino Kleina, Ryoichiro Kageyamab, et al.
During early pancreatic development, Notch signaling represses differentiation of endocrine cells and promotes proliferation of Nkx6-1+Ptf1a+ multipotent progenitor cells (MPCs). Later, antagonistic interactions between Nkx6 transcription factors and Ptf1a function to segregate MPCs into distal Nkx6-1−Ptf1a+ acinar progenitors and proximal Nkx6-1+Ptf1a− duct and β-cell progenitors. Distal cells are initially multipotent, but evolve into unipotent, acinar cell progenitors. Conversely, proximal cells are bipotent and give rise to duct cells and late-born endocrine cells, including the insulin producing β-cells. However, signals that regulate proximodistal (P-D) patterning and thus formation of β-cell progenitors are unknown. Here we show that Mind bomb 1 (Mib1) is required for correct P-D patterning of the developing pancreas and β-cell formation. We found that endoderm-specific inactivation of Mib1 caused a loss of Nkx6-1+Ptf1a− and Hnf1β+ cells and a corresponding loss of Neurog3+ endocrine progenitors and β-cells. An accompanying increase in Nkx6-1−Ptf1a+ and amylase+ cells, occupying the proximal domain, suggests that proximal cells adopt a distal fate in the absence of Mib1 activity. Impeding Notch-mediated transcriptional activation by conditional expression of dominant negative Mastermind-like 1 (Maml1) resulted in a similarly distorted P-D patterning and suppressed β-cell formation, as did conditional inactivation of the Notch target gene Hes1. Our results reveal iterative use of Notch in pancreatic development to ensure correct P-D patterning and adequate β-cell formation.
