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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

Project description:LCM-coupled nanoPOTS proteomics using FAIMS of intra-islet microstructures. 5 acinar samples, 5 whole islets, 5 islet interface vasculature pools, 5 islet inner microvasculature pools, 3 islets after microsvasculature removed.

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Effects Beta-hydroxybutyrate on human islet proteome

Project description:We measured changes in the human islet proteome following 72-hr exposure to 3 mM R-beta-hydroxybutyrate. Islets from 12 metabolically healthy human islet donors were obtained from the Alberta Diabetes Institute Islet Core

2024-06-17 | MSV000095058 | MassIVE

Nutrient regulation of the islet epigenome controls adaptive insulin secretion

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.

2023-02-24 | GSE134901 | GEO

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

Project description:Using intravital 2-photon islet imaging we show that T cell extravasation into the islets is an extended process, with T cells arresting in the islet vasculature in close proximity to perivascular CD11c+ cells. Antigen is not required for T cell trafficking to infiltrated islets, but T cell chemokine receptor signaling is necessary. Using RNAseq, we show that islet CD11c+ cells express over 20 different chemokines that bind chemokine receptors expressed on islet T cells.

2019-03-01 | GSE121804 | GEO

Proteomic pathways to metabolic disease and type 2 diabetes in the pancreatic islet

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.

2021-10-08 | PXD024522 | Pride

Identification and analysis of pancreatic islet specific enhancers

Project description:We anticipated that the identification of cis-regulatory regions active in pancreatic islets would help increase our understanding of islet biology and the pathology of diabetes. Towards this end we used histone H3 lysine 4 monomethylation-based nucleosome predictions genome-wide, in conjunction with binding data for PDX1, FOXA2, MAFA, and NEUROD1, to identify 3,654 putative enhancers that are H3K4me1-enriched uniquely in islets as compared to 14 other tissue or cell-types. We show that these islet-specific enhancers are associated with genes with significantly higher islet specificity than genes associated with non-specific enhancers. Further, islet-specific enhancers were not enriched for typical active or repressive histone methylations in embryonic stem cells and liver, suggesting they are formed by de novo histone methylation during pancreas development. We also identify a subset of enhancers bivalently marked by both H3K4me1 and H3K27me3 in adult pancreatic islets. Further, we show that islet-specific enhancers triple- or quadruple- bound by PDX1, MAFA, NEUROD1 and/or FOXA2 are associated with genes with particularly high islet-specificity, and that these loci are enriched in regions with functional activity in islet cell types. Finally, we demonstrate that cytokines reduce H3K4me1 enrichment levels at selected triple- or quadruple-bound islet-specific enhancers, suggesting that epigenetic changes may contribute to cytokine-induced b-cell dysfunction. In conjunction with data from Hoffman et al Genome Research 2010, an analysis of histone modifications and transcription factor binding sites to identify enhancer regions

2011-06-30 | E-GEOD-30298 | biostudies-arrayexpress

Transcription profiling of pancreatic islet implanted transgenic (expressing survivini) in mice

Project description:Transgenic mice were generated that expressed the inhibitor of apoptosis and mitotic regulator survivin in pancreatic islet beta cells. Control non-transgenic or transgenic islets were then used in a model of islet transplantation in diabetic recipient mice and tested for their ability to correct hyperglycemia and allow long-term engraftment of tranplanted islets in vivo. Control or transgenic islets were analyzed by chip microarray for potential transcriptional changes associated with transgenic expression of survivin, in vivo.

2006-01-16 | E-MEXP-536 | biostudies-arrayexpress

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).

2007-04-06 | E-CBIL-27 | biostudies-arrayexpress

Human islet of Langerhans grown on nanosubstrates LC-MSMS

Project description:Intensive efforts are focused on identifying regulators of human pancreatic islet cell growth and maturation to accelerate development of therapies for diabetes. In the present study we evaluate the contribution of the physical properties of the extracellular matrix in supporting long term culture of human islets in vitro. We used metal oxide layers with tailored nanoscale roughness to fabricate scaffolds. Their suitability to support long term culture of human islets was investigated through assessment of β-cell survival, differentiation and function by using a proteomic approach to evaluate the molecular mechanisms involved. Proteomic analysis confirmed that ns-ZrOx promoted the activation of a transcriptional and translational program leading to activation of pro-survival and pro-differentiation signalling pathways. The process was driven by a mechanotransductive pathway driven by nanostructured topology, via remodelling of the actin cytoskeleton nuclear architecture and increase of oxygen sensor PDH2 Our data suggest that β-cells relay on nanotopography features to regulate their differentiation and survival. Tailored nanostructured substrates may provide a unique strategy to identify novel hints for tissue engineering and molecular /pharmacological targets of intervention to treat diabetes mellitus.

2018-07-11 | PXD007569 | Pride

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