Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

43 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Serum starvation effects on human Islet-derived Precursor Cells

ABSTRACT: This is an Affy experiment that was conducted on human derived pancreatic islet cells that were expanded in serum-containing medium to produce hIPC cells (human Islet-derived Precursor Cells). These cells, when subjected to 1 day of serum starvation, transition into hormone-expressing ICAs (Islet-like Cell Aggregates). In this experiment, proliferative hIPCs were trypsin-harvested and transferred in either serum-containing media (C) or serum-free media (F). After 24 hours, cells from both conditions were harvested and RNA was extracted. This experiment was meant to identify gene expression changes between hIPC early differentiation (condition F) and hIPC proliferation (condition C) with cells being in culture for the same amount of time. There were 3 replicates each for each of the two conditions, of which the 3rd was a pool of the first 2 replicates.

INSTRUMENT(S): Affymetrix GeneChip Scanner 3000 (GCS3000)

ORGANISM(S): Homo sapiens

SUBMITTER: Gershengorn Marvin

PROVIDER: E-MTAB-2936 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

microRNA expression profile in isolated human pancreatic islets and in human pancreatic islet-derived extracellular vesicles -EVs-

Project description:Human pancreatic islets were isolated from pancreas of deceased donors by Ricordi's procedure and cultured in CMRL 1066 medium additioned with human albumin. EVs were isolated from conditioned medium derived from islet culture after isolation. Once isolated, RNA of islets and islet-derived EVs was extracted and analyzed for microRNA expression within 48 hours after isolation.

2012-07-30 | E-MEXP-3691 | biostudies-arrayexpress

Insulin-producing cells generated from dedifferentiated human pancreatic beta cells expanded in vitro

Project description:Expansion of beta cells from the limited number of adult human islet donors is an attractive prospect for increasing cell availability for cell therapy of diabetes. However, while evidence supports the replicative capacity of adult beta cells in vivo, attempts at expanding human islet cells in tissue culture resulted in loss of beta-cell phenotype. Using a genetic lineage-tracing approach we have provided evidence for massive proliferation of beta-cell-derived (BCD) cells within these cultures. Expansion involves dedifferentiation resembling epithelial-mesenchymal transition (EMT). Epigenetic analyses indicate that key beta-cell genes maintain a partially open chromatin structure in expanded BCD cells, although they are not transcribed. Here we report that BCD cells can be induced to redifferentiate by a combination of soluble factors. The redifferentiated cells express beta-cell genes, store insulin in typical secretory vesicles, and release it in response to glucose. The redifferentiation process involves mesenchymal-epithelial transition, as judged from changes in gene expression. Moreover, inhibition of the EMT effector SLUG using shRNA results in stimulation of redifferentiation. BCD cells also give rise at a low rate to cells expressing other islet hormones, suggesting transition through an islet progenitor-like stage during redifferentiation. These findings suggest that ex-vivo expansion of adult human islet cells is a promising approach for generation of insulin-producing cells for transplantation, as well as basic research, toxicology studies, and drug screening. Gene expression was studied in unexpanded islets (4 donors), expanded and dedifferentiated islet cells (4 donors), and re-differentiated islet cells (3 donors). The experiment was performed in 3 batches (see Date in the description table below).

2011-07-18 | E-GEOD-30732 | biostudies-arrayexpress

transcriptional profile of islet EVs for diabetes genes

Project description:Identification of transcriptional profile of several genes involved in diabetes in islet-derived extracellular vesicles (Evs). Recently, EVs are identified as a new mechanism in cell-to-cell communication by transfer of protein and genic information (mRNA, microRNA). Their role is under investigation in immunology, stem cell and cancer, but not in islets and diabetes. The aim of this experiment is to identify mRNA transcripts (in particular, mRNA transcripts involved in diabetes pathophysiology) present in islet Evs.

2012-08-02 | E-MEXP-3695 | biostudies-arrayexpress

Global transcriptomic analysis of human pancreatic islets reveals novel genes influencing glucose metabolism [expression array]

Project description:Here we harnessed the potential of expression arrays in 89 human pancreatic islet donors (different levels of blood glucose (HbA1c)) to identify genes regulated in this relevant tissue for type 2 diabetes (T2D). Islets from cadaver donors were provided by the Nordic Islet Transplantation Programme (www.nordicislets.org), Uppsala University. The microarrays were performed using GeneChipM-BM-. Human Gene 1.0 ST whole transcript according to Affymetrix standard protocol.

2014-07-17 | E-GEOD-50397 | biostudies-arrayexpress

Gene expression from human pancreatic islet

Project description:Expression profiling of cell cycle genes in human pancreatic islets with and without type 2 diabetes Islets from cadaver donors were provided by the Nordic Islet Transplantation Programme (www.nordicislets.org), Uppsala University. The microarrays were performed using GeneChipM-BM-. Human Gene 1.0 ST whole transcript according to Affymetrix standard protocol.

2013-03-15 | E-GEOD-44035 | biostudies-arrayexpress

Transcription profiling of human cholangiocarcinoma cells (cholangiocytes) expressing IL-6

Project description:The association between chronic inflammation and the development and progression of malignancy is exemplified in the biliary tract where persistent inflammation strongly predisposes to cholangiocarcinoma. The inflammatory cytokine interleukin-6 (IL-6) enhances tumor growth in cholangiocarcinoma by altered gene expression via autocrine mechanisms. We therefore investigated the effect of chronic exposure to IL-6 on gene expression using malignant cholangiocytes stably transfected to overexpress IL-6. Comparison of gene expression identified several genes that were altered by enforced IL-6 expression. Experiment Overall Design: Mz-ChA-1 cells were stably transfected with a pTarget vector plasmid containing full length IL-6 under the control of a CMV promoter to generate Mz-IL6. Cells transfected with empty vector were used as control

2008-10-21 | E-GEOD-11883 | biostudies-arrayexpress

MicroRNA expression profiling of human pancreatic islets reveals microRNAs with altered expression due to glyceamic status

Project description:Global microRNA (miRNA) profiling was performed in 18 human islet donors using Exiqon’s LNA (locked nucleic acid)-based array platform. Donors were divided into three groups according to their HbA1c levels and type-2 diabetes diagnosis (normal glucose tolerance - NGT, impaired glucose tolerance - IGT, diagnosed with type-2 diabetes-T2D). To identify miRNAs with altered expression due to glyceamic status, donors were matched for age, gender and BMI and differential expression analysis was performed in 7 NGT vs 7 IGT/T2D donors using Significance Analysis of Microarrays (SAM) based on False Discovery Rate (FDR) statistics.

2022-02-28 | E-MTAB-11125 | biostudies-arrayexpress

Expression data from human pancreatic islets

Project description:A gene co-expression network analysis has been conducted to identify T2D-associated gene modules. Donors 1-48 were used for the initial analysis and donors 49-80 for the replication and were normalized separately in this study Islets from cadaver donors (57 non-diabetic and 20 diabetic) were provided by the Nordic Islet Transplantation Programme (www.nordicislets.org), Uppsala University. The microarrays were performed using GeneChipM-BM-. Human Gene 1.0 ST whole transcript according to Affymetrix standard protocol.

2012-10-23 | E-GEOD-41762 | biostudies-arrayexpress

Open chromatin mapping identifies transcriptional networks regulating human epididymis epithelial function [Agilent expression]

Project description:The epithelium lining the epididymis in the male reproductive tract maintains a luminal environment that promotes sperm cell maturation. This process is dependent on the coordinated expression of many genes that encode proteins with a role in epithelial transport. We previously generated genome-wide maps of open chromatin in primary human fetal epididymis epithelial cells to identify potential regulatory elements controlling coordinated gene expression in the epididymis epithelium. Subsequent in silico analysis identified transcription factor binding sites (TFBS) that were over-represented in the HEE open chromatin, include the motif for paired box 2 (PAX2). PAX2 is a critical transcriptional regulator of urogenital tract development, which is well studied in the kidney but is unexplored in the epididymis. Due to the limited lifespan of primary HEE cells in culture we investigated the role of PAX2 in an immortalized HEE cell line (REP). First, REP cells were evaluated by DNase-seq and their open chromatin map overlapped that of primary HEE cells at ~ 65% of sites. Moreover, the PAX2-binding motif was again identified as an overrepresented TFBS within intergenic open chromatin, though on fewer chromosomes than in the primary HEE cells. To identify PAX2-target genes in REP cells, RNA-seq analysis was performed after siRNA-mediated depletion of PAX2 in comparison to a non-targeting siRNA. In response to PAX2-represssion, 3142 transcripts were differentially expressed (1334 up-regulated and 1808 down-regulated). Novel PAX2 targets included multiple genes encoding proteins with a predicted function in the epididymis epithelium. Gene expression in REP cells was measured at 16 hours after exposure to 1nM R1881 or vehicle control.

2015-01-07 | E-GEOD-60381 | biostudies-arrayexpress

Redifferentiation of adult human M-NM-2 cells expanded in vitro by inhibition of the WNT pathway

Project description:In vitro expansion of adult human islet M-NM-2 cells is an attractive solution for the shortage of tissue for cell replacement therapy of type 1 diabetes. Using a lineage tracing approach, we have demonstrated that M-NM-2-cell-derived (BCD) cells rapidly dedifferentiate in culture and can proliferate for up to 16 population doublings. Dedifferentiation is associated with changes resembling epithelial-mesenchymal transition (EMT). The WNT pathway has been shown to induce EMT and plays key roles in regulating replication and differentiation in many cell types. Here we show that BCD cell dedifferentiation is associated with M-NM-2-catenin translocation into the nucleus and activation of the WNT pathway. Inhibition of M-NM-2-catenin expression in expanded BCD cells using short hairpin RNA resulted in growth arrest, mesenchymal-epithelial transition, and redifferentiation, as judged by activation of M-NM-2-cell gene expression. Furthermore, inhibition of M-NM-2-catenin expression synergized with redifferentiation induced by a combination of soluble factors, as judged by an increase in the number of C-peptide-positive cells. Simultaneous inhibition of the WNT and NOTCH pathways also resulted in a synergistic effect on redifferentiation. These findings, which were reproducible in cells derived from multiple human donors, suggest that inhibition of the WNT pathway may contribute to a therapeutically applicable way for generation of functional insulin-producing cells following ex-vivo expansion. Gene expression was studied for beta-cells (4 donors). Dedifferentiation was induced by inhibition of M-NM-2-catenin expression using shRNA. The experiment was performed in 4 batches (see the 'Date' characteristic in the Sample records).

2014-08-27 | E-GEOD-60803 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data