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Robust Differentiation of Islet Progenitors into Functional Insulin-secreting Cells by Suppression of Key Transcription Regulators

ABSTRACT: Gene profiling revealed that differentiation was accompanied by suppression of a range of transcription regulator genes typical of islet progenitor cells. In order to understand molecular mechanisms of differentiation, transcriptome-wide gene expression analysis was performed on purified islet progenitors at days 0, 1 and 4 of differentiation together with adult islets as a control.

ORGANISM(S): Mus musculus

PROVIDER: GSE51944 | GEO | 2013/11/01

SECONDARY ACCESSION(S): PRJNA225884

REPOSITORIES: GEO

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Robust Differentiation of Islet Progenitors into Functional Insulin-secreting Cells by Suppression of Key Transcription Regulators

Project description:Gene profiling revealed that differentiation was accompanied by suppression of a range of transcription regulator genes typical of islet progenitor cells. In order to understand molecular mechanisms of differentiation, transcriptome-wide gene expression analysis was performed on purified islet progenitors at days 0, 1 and 4 of differentiation together with adult islets as a control. In order to understand molecular mechanisms of differentiation, transcriptome-wide gene expression analysis was performed on purified islet progenitors at days 0, 1 and 4 of differentiation together with adult islets as a control.

2013-11-01 | E-GEOD-51944 | biostudies-arrayexpress

Proteomic profiling of intra-islet features reveals substructure-specific protein signatures

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Project description:Adaptation of the islet β-cell insulin secretory response to changing insulin demand is critical for blood glucose homeostasis, yet the mechanisms underlying this adaptation are unknown. Here, we show that nutrient cues adapt insulin secretion by modulating chromatin state and transcription of genes regulating β-cell nutrient sensing and metabolism. Feeding stimulates histone acetylation at sites occupied by the chromatin-modifying enzyme Lsd1 in islets. We demonstrate that β-cell-specific deletion of Lsd1 leads to insulin hypersecretion, aberrant expression of nutrient response genes, and histone hyperacetylation, features we also observed in the db/db model of chronically increased insulin demand. Moreover, genetic variants associated with fasting glucose levels and type 2 diabetes risk are enriched at LSD1-bound sites in human islets, suggesting interindividual variation in β-cell functional adaptation in humans. These findings reveal nutrient state-dependent modulation of the islet epigenome and identify Lsd1 as a regulator of feeding-stimulated chromatin modification and adaptive insulin secretion.

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Effects Beta-hydroxybutyrate on human islet proteome

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RNAseq of Islet CD11c+ cells and Islet T cells from 12-20 week non-obese diabetic mice

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Project description:Pancreatic islets are essential for maintaining physiological blood glucose levels, and declining islet function is a hallmark of type 2 diabetes. Here we employ mass spectrometry (MS)-based proteomics to systematically analyse purified islets from 9 genetic or diet-induced mouse models representing a broad cross-section of metabolic health. Quantifying the islet proteome to a depth of >11,500 proteins, this study represents the most detailed analysis of islet proteins to date. Our data highlight that the vast majority of islet proteins are expressed in all strains and diets, but more than half of the proteins vary in expression levels. Associating these varied protein expression levels on an individual animal basis with individual phenotypic measures reveals islet mitochondrial function as a major positive indicator of metabolic health. This compendium of strain-specific and dietary changes to mouse islet proteomes represents a comprehensive resource for basic and translational islet cell biology.

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Identification and analysis of pancreatic islet specific enhancers

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Transcription profiling of cultured normal human islet tissue, islets treated with interferon alpha 2 beta, islet-depleted exocrine pancreas, pancreas, liver and kidney tissue

Project description:The purpose of this study was to identify mRNA transcripts encoding tissue restricted cell surface proteins on human islet tissue that, in turn, might serve as markers for determination of healthy, transplanted and/or diseased islet cell mass. Using oligonucleotide microarrays and clinical grade human islets, we obtained the gene expression profiles of cultured normal islet tissue and compared them to profiles of islets treated with interferon alpha 2 beta, islet-depleted exocrine pancreas, pooled whole pancreas, pooled liver and pooled kidney tissue. Data set filtering and comparisons of gene expression patterns revealed a small set of genes corresponding to transmembrane or membrane associated proteins with limited tissue distributions (present in Islets of Langerhans and, often, central or peripheral nervous system tissues, but absent from exocrine pancreas, liver, kidney and other tissues) with possible utility as novel islet markers. Under the influence of IFN alpha, some of these transcripts show differential expression as confirmed by real time PCR. In addition, we found significant differential expression of two sets of transcripts expressed in islets but with broad tissue distributions, non classical MHC class I b (HLA-G and F) and MHC Class II locus (e.g. HLA-DR alpha and HLA-DQ alpha and beta).

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