کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5511363 | 1539854 | 2017 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Dnmt1 activity is dispensable in δ-cells but is essential for α-cell homeostasis
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کلمات کلیدی
DOXEZH2Dnmt1DNA methyltransferase 1rtTAYFPα-cellsIAPDTRCREGCGPRCSSTINSinsulin - انسولینtetO - تتوenhancer of zeste homolog 2 - تقویت کننده یا ژنتیک همولوگ 2diphtheria toxin - توکسین دیفتریPancreatic islet - جزیره پانکراسdoxycycline - داکسی سایکلینintracisternal A-particle - ذره ای داخل شکمیSomatostatin - سوماتواستاتینpolycomb repressive complex - مجتمع سرکوبگر پلی کامبRIP - پاره کردنyellow fluorescent protein - پروتئین فلورسنت زردrat insulin promoter - پروموتر انسولین موشCre recombinase - کرم recombinaseGlucagon - گلوکاگونDiphtheria Toxin Receptor - گیرنده توکسین دیفتری
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
In addition to β-cells, pancreatic islets contain α- and δ-cells, which respectively produce glucagon and somatostatin. The reprogramming of these two endocrine cell types into insulin producers, as observed after a massive β-cell ablation in mice, may help restoring a functional β-cell mass in type 1 diabetes. Yet, the spontaneous α-to-β and δ-to-β conversion processes are relatively inefficient in adult animals and the underlying epigenetic mechanisms remain unclear. Several studies indicate that the conserved chromatin modifiers DNA methyltransferase 1 (Dnmt1) and Enhancer of zeste homolog 2 (Ezh2) are important for pancreas development and restrict islet cell plasticity. Here, to investigate the role of these two enzymes in α- and δ-cell development and fate maintenance, we genetically inactivated them in each of these two cell types. We found that loss of Dnmt1 does not enhance the conversion of α- or δ-cells toward a β-like fate. In addition, while Dnmt1 was dispensable for the development of these two cell types, we noticed a gradual loss of α-, but not δ-cells in adult mice. Finally, we found that Ezh2 inactivation does not enhance α-cell plasticity, and, contrary to what is observed in β-cells, does not impair α-cell proliferation. Our results indicate that both Dnmt1 and Ezh2 play distinct roles in the different islet cell types.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: The International Journal of Biochemistry & Cell Biology - Volume 88, July 2017, Pages 226-235
Journal: The International Journal of Biochemistry & Cell Biology - Volume 88, July 2017, Pages 226-235
نویسندگان
Nicolas Damond, Fabrizio Thorel, Seung K. Kim, Pedro L. Herrera,