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2015年6月11日 讯 /生物谷BIOON/ –近日，刊登在国际杂志Islets上的一篇研究论文中，来自博里汉姆扬大学的研究人员通过研究发现，一种特殊基因或可帮助阐明糖尿病发病的根源；目前在全球范围内高血糖影响着4亿人的健康，为了深入研究这种特殊基因的功能，研究人员转向了对患糖尿病的学生进行研究。
文章中研究者对4名患有1型糖尿病的学生进行研究，学生患病和饮食及生活方式均无关联，研究者Tessem说道，这项研究中我们调查了可以激活胰岛β细胞的分子途径，β细胞是可以产生胰岛素的胰腺细胞，然而在1型糖尿病中这些细胞往往会被机体免疫系统所攻击并破坏。文章中所发现的特殊基因不仅可以促进β细胞复制，而且可以帮助其维持识别葡萄糖及分泌胰岛素的能力。
研究者的目的是想鉴别出所有可以促进β细胞复制的基因，这或许就可以帮助研究人员设计新型药物来激活或关闭这些特殊基因的表达；如果给予糖尿病患者β细胞或许就可以帮助治疗患者的疾病；当前将β细胞植入到糖尿病患者体内的方法包括将产生β细胞的小岛植入到患者机体中，而为了使得植入的胰岛产生足够的β细胞，一位患者或许需要两个小岛结构。
因此理解诱导β细胞生长的途径或许可以帮助降低患者对胰岛的需求，从而就为开发新型疗法来促进β细胞的复制生长提供一定的帮助；当然研究者同时还指出，我们并不必担心胰岛素的注射或者血糖升高，本文研究对于理解个体患糖尿病的发病机制，以及后期开发特殊疗法来预防及治疗糖尿病将带来巨大帮助。（基因宝jiyinbao.com）
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Aurora Kinase A is critical for the Nkx6.1 mediated β-cell proliferation pathway
Amanda Hobsona, Carrie Draneya, Andrew Stratforda, Thomas C Beckerb, Danhong Lub, Michelle Arlottob & Jeffery S Tessema*
Type 1 and type 2 diabetes are ultimately characterized by depleted β-cell mass. Characterization of the molecular pathways that control β-cell proliferation could be harnessed to restore these cells. The homeobox β-cell transcription factor Nkx6.1 induces β-cell proliferation by activating the orphan nuclear receptors Nr4a1 and Nr4a3. Here, we demonstrate that Nkx6.1 localizes to the promoter of the mitotic kinase AURKA (Aurora Kinase A) and induces its expression. Adenovirus mediated overexpression of AURKA is sufficient to induce proliferation in primary rat islets while maintaining glucose stimulated insulin secretion. Furthermore, AURKA is necessary for Nkx6.1 mediated β-cell proliferation as demonstrated by shRNA mediated knock down and pharmacological inhibition of AURKA kinase activity. AURKA preferentially induces DNA replication in β-cells as measured by BrdU incorporation, and enhances the rate of histone H3 phosphorylation in primary β-cells, demonstrating that AURKA induces the replicative and mitotic cell cycle phases in rat β-cells. Finally, overexpression of AURKA results in phosphorylation of the cell cycle regulator p53, which targets p53 for degradation and permits cell cycle progression. These studies define a pathway by which AURKA upregulation by Nkx6.1 results in phosphorylation and degradation of p53, thus removing a key inhibitory factor and permitting engagement of the β-cell proliferation pathway.