Expression data from type 2 diabetic and non-diabetic isolated human islets
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Marco Bugliani
PROVIDER: E-GEOD-25724 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Diabetic islets
2009-06-30 | E-MEXP-1878 | biostudies-arrayexpress
Project description:We performed microarray analysis to evaluate differences in the transcriptome of type 2 diabetic human islets compared to non-diabetic islet samples.
2010-12-01 | GSE25724 | GEO
Project description:Hybrid insulin peptides (HIPs) result from the linkage of an insulin C-peptide fragment and another peptide via a traditional peptide bond to generate a sequence that is not encoded in the genome. Here, we sought to identify HIPs naturally present in the pancreatic islets of non-obese diabetic (NOD) mice, BALB/c mice, and non-diabetic human donors by mass spectrometry.
2019-01-07 | PXD011606 | Pride
Project description:Progressive decline of pancreatic beta cell function is central to the pathogenesis of type 2 diabetes. Protein phosphorylation regulates glucose-stimulated insulin secretion from beta cells, but how signaling networks are remodeled in diabetic islets in vivo remains unknown. Using high-sensitivity mass spectrometry-based proteomics we quantified 6,500 proteins and 13,000 phosphopeptides in islets of obese diabetic mice and matched controls, revealing drastic remodeling of key kinase hubs and signaling pathways. Integration with a literature-derived signaling network implicated GSK3 kinase in the control of the beta cell-specific transcription factor PDX1. Deep phosphoproteomic analysis of human islets chronically treated with high glucose demonstrated a conserved glucotoxicity-dependent role of GSK3 kinase in regulating insulin secretion. Remarkably, the ability of beta cells to secrete insulin in response to glucose was rescued almost completely by pharmacological inhibition of GSK3. Thus, our resource enables investigation of mechanisms and drug targets in type 2 diabetes.
2019-03-15 | PXD012671 | Pride
Project description:Purpose: Myt3 is a putative pro-survival factor in pancreatic islets and is expressed from E18.5 onwards. The genes that Myt3 regulates and its role in islet-cell development, function and survival are not fully known. The purpose of this study was to determine the changes in gene expression following the suppression or over-expression of Myt3 to identify possible pathways that may be regulated by Myt3. Methods: Pancreatic islets were isolated from both male and female C57/B6 mice by collagenase digestion and were picked by hand. Hand-picked islets were plated onto 804G, a complete extracellular-matrix (ECM) produced by a rat bladder carcinoma cell line, treated tissue culture dishes and transduced with 1x106 pfu virus overnight. The next day media was changed to fresh RPMI and islets were cultured for 7 days. At the end of the culture period islets were dispersed and FACs sorted for GFP+ cells. Sorted cells from at least 5 experiments were pooled and RNA was isolated using Trizol reagent. 800ng of RNA was used in the Illumina TruSeq kit for library preparation. Results: Comparison of gene expression levels between control-transduced islets and either shMyt3- or Myt3-transduced islets resulted in the identification of 51 and 89 significantly altered genes respectively. Conclusions: Our study represents the first comprehensive analysis of genes that are potentially regulated by Myt3 and highlight potential pathways that are likely important for mediating Myt3's effects of islet development, function and survival.
2015-07-10 | GSE70699 | GEO
Project description:Long non-coding RNAs (LncRNAs) constitute an extensive fraction of the mammalian transcriptome. In this study, lncRNAs dysregulated in the islets of diabetic db/db mice were identified by high-throughput RNA sequencing. More than 1600 lncRNAs were detected using RNA sequencing, indicating that lncRNAs were abundant in islets. Among them, we found that lncRNA-Malat1 was significantly reduced in diabetic mouse islets. Further experiments suggested an involvement of lncRNA-Malat1 in lipotoxicity-induced β-cell dysfunction.
2022-11-01 | GSE139823 | GEO
Project description:Type 2 diabetes mellitus (T2DM) is a complex disease characterized by the inability of the insulin-producing β-cells in the endocrine pancreas to overcome insulin resistance in peripheral tissues. To determine if microRNAs are involved in the pathogenesis of human T2DM, we sequenced the small RNAs of human islets from diabetic and non-diabetic organ donors. We identified a cluster of miRNAs in an imprinted locus on human chromosome 14q32 that is highly and specifically expressed in human β-cells and dramatically down-regulated in islets from T2DM organ donors. The down-regulation of this locus strongly correlates with hyper-methylation of its promoter. Using HITS-CLIP for the essential RISC-component Argonaute, we identified disease-relevant targets of the chromosome 14q32 microRNAs, such as IAPP and TP53INP1 that cause increased β-cell apoptosis upon over-expression in human islets. Our results support a role for microRNAs and their epigenetic control by DNA methylation in the pathogenesis of T2DM. Identification of miRNA-target interaction in human islets using HITS-CLIP, one mRNA library and one miRNA library
2013-11-22 | E-GEOD-51924 | biostudies-arrayexpress
Project description:Type 2 diabetes mellitus (T2DM) is a multi-factorial disease characterized by the inability of beta-cells in the endocrine pancreas to produce sufficient amounts of insulin to overcome insulin resistance in peripheral tissue. To investigate the function of miRNAs in T2DM, we sequenced the small RNAs of human islets cells from diabetic and non-diabetic organ donors and identified a cluster of miRNAs in an imprinted locus on human chromosome 14 to be dramatically down-regulated in T2DM islets. These miRNAs are highly and specifically expressed in human beta-cells. The down-regulation of this imprinted locus strongly correlates with increased methylation of its promoter in T2DM islets, providing evidence for an epigenetic modification that contributes to the pathogenesis of T2DM. Targets of the Chr 14q32 cluster of miRNAs were identified by high-throughput sequencing of cross-linked and immunoprecipitated RNA (HITS-CLIP) of Argonaute. We have also identified a unique class of sequences, termed chimeric reads, that represent an in vivo ligation of miRNAs and their targets while in complex with Argonaute, and which allow for the direct identification of miRNA:target relationships in vivo. There are three experiments in this submission. All are in human islets or islet cell types. The first is a comparison of miRNA levels in sorted alpha versus beta cells. There is one replicate for this experiment. The second experiment is to measure the expression of miRNAs in whole islets as a function of glucose levels. There are three levels and one replicate for each condition. The third exeriment is a comparison of whole islets taken from human donors that were suspected/confirmed Type 2 diabetic or considered controls. There are 3 controls and 4 T2D samples.
2013-12-01 | E-GEOD-52314 | biostudies-arrayexpress
Project description:Purpose: Myt3 is a putative pro-survival factor in pancreatic islets and is expressed from E18.5 onwards. The genes that Myt3 regulates and its role in islet-cell development, function and survival are not fully known. The purpose of this study was to determine the changes in gene expression following the suppression or over-expression of Myt3 to identify possible pathways that may be regulated by Myt3. Methods: Pancreatic islets were isolated from both male and female C57/B6 mice by collagenase digestion and were picked by hand. Hand-picked islets were plated onto 804G, a complete extracellular-matrix (ECM) produced by a rat bladder carcinoma cell line, treated tissue culture dishes and transduced with 1x106 pfu virus overnight. The next day media was changed to fresh RPMI and islets were cultured for 7 days. At the end of the culture period islets were dispersed and FACs sorted for GFP+ cells. Sorted cells from at least 5 experiments were pooled and RNA was isolated using Trizol reagent. 800ng of RNA was used in the Illumina TruSeq kit for library preparation. Results: Comparison of gene expression levels between control-transduced islets and either shMyt3- or Myt3-transduced islets resulted in the identification of 51 and 89 significantly altered genes respectively. Conclusions: Our study represents the first comprehensive analysis of genes that are potentially regulated by Myt3 and highlight potential pathways that are likely important for mediating Myt3's effects of islet development, function and survival. Isolated islets were transduced with adenoviruses, cultured for 7 days on ECM and FACS sorted. Cells from up to 5 experiments were pooled and sequenced.
2015-07-10 | E-GEOD-70699 | biostudies-arrayexpress
Project description:microRNA Expression in Normal and Diabetic Pancreatic Islets
| PRJNA807330 | ENA