Murine Perinatal β-Cell Proliferation and the Differentiation of Human Stem Cell-Derived Insulin-Expressing Cells Require NEUROD1.
作者： Anthony I. Romer , Ruth A. Singer , Lina Sui , Dieter Egli , Lori Sussel
DOI: 10.2337/DB19-0117
关键词: Biology 、 Transcription factor 、 Cell culture 、 Cell growth 、 Transgene 、 Cell biology 、 Embryonic stem cell 、 Stem cell 、 Progenitor cell 、 NEUROD1
摘要: Inactivation of the β-cell transcription factor NEUROD1 causes diabetes in mice and humans. In this study, we uncovered novel functions during murine islet cell development differentiation human embryonic stem cells (HESCs) into insulin-producing cells. mice, determined that Neurod1 is required for perinatal proliferation α- β-cells. Surprisingly, apoptosis only makes a minor contribution to loss when deleted. HESCs severely impaired their from pancreatic progenitors insulin-expressing (HESC-β) cells; however, survival or was not affected at time points analyzed. also HESC-β full activation an essential network. These data reveal conserved distinct mouse maturation, with important implications about function diabetes.
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