Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from rat INS-1E cells

ABSTRACT: Cytokine-induced beta-cell apoptosis is a key event for the death of pancreatic beta cells in the development of type-1 diabetes. We identified BRD0476 as a novel suppressor of cytokine-induced beta-cell apoptosis. We used microarrays to look for gene set(s) that are regulated by BRD0476.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE42897 | GEO | 2012/12/14

SECONDARY ACCESSION(S): PRJNA183731

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Expression data from rat INS-1E cells

Project description:Cytokine-induced beta-cell apoptosis is a key event for the death of pancreatic beta cells in the development of type-1 diabetes. We identified BRD0476 as a novel suppressor of cytokine-induced beta-cell apoptosis. We used microarrays to look for gene set(s) that are regulated by BRD0476. Rat INS-1E cells were treated with cytokine cocktails (IL-1b, IFN-g and TNF-a) and/or BRD0476 for 6 or 12 hours. Total RNAs were isolated using the RNEasy kit from Qiagen.

2012-12-14 | E-GEOD-42897 | biostudies-arrayexpress

Rat insulin-producing INS-1E exposed to cytokines IL-1β and IFN-γ

2013-12-19 | GSE53453 | GEO

Rat insulin-producing INS-1E exposed to cytokines IL-1β and IFN-γ

Project description:In the context of T1 Diabetes, pro-inflammatory cytokines IL-1β and IFN-γ are known to contribute to β-cell apoptosis; The measurement of mRNA expression following β-cell exposure to these cytokines gives a picture of the changes in gene expression characterizing the path to β-cell dysfunction and death. INS1 cell lines were cultured in medium with or without IL-1β and IFN-γ. The samples were collected at various time points for profiling with Affymetrix Rat ST arrays. These experiments were performed on two separate occasions.

2013-12-19 | E-GEOD-53453 | biostudies-arrayexpress

Transcription profiling of rat insulinoma-beta (INS-1E) cells exposed to the cytokines IL-1-beta and IFN-gamma for six different lengths of time and with or without the inducible NO synthase blocker NMA

Project description:Locally released cytokines contribute to beta cell dysfunction and apoptosis in Type 1 diabetes. In vitro exposure of insulin producing INS-1E cells to the cytokines interleukin (IL)-1beta + interferon (IFN) gamma leads to a significant increase in apoptosis. To characterize the genetic networks implicated in beta cell dysfunction and apoptosis and its dependence on nitric oxide (NO) production, we performed a time course analysis using the Affymetrix RG U34A microarry. INS-1E cells were exposed in duplicate to IL-1beta + IFN-gamma for six different time points (1, 2, 4, 8, 12, and 24 h) with or without the inducible NO synthase blocker.

2006-06-14 | E-CBIL-10 | biostudies-arrayexpress

Transcription profiling of rat pancreatic beta-cells in response to cytokine exposure and NF-kappa B activation blocking

Project description:Type 1 diabetes mellitus results from an autoimmune destruction of pancreatic beta-cells. Based on findings suggesting NF-kappa B plays a role in beta cell apoptosis, we blocked NF-kappa B activation in cytokine-exposed FACS sorted beta cells by a recombinant adenovirus (AdI kappa B((SA)2)) containing an inhibitor of NF kappa B alpha (I kappa Bac) super-repressor (S32A/S36A). The expression profile was then analyzed with the Affymetrix RG U34a microarray.

2006-06-16 | E-CBIL-9 | biostudies-arrayexpress

Sfrp5 increases glucose-stimulated insulin secretion in the rat pancreatic beta cell line INS-1E.

Project description:Previous studies reported that secreted frizzled-related protein-5 (Sfrp5) decreases beta cell proliferation and increases fasting insulin levels, but studies on direct effects of Sfrp5 on insulin secretion and its underlying mechanisms are missing. This study examined effects of Sfrp5 on (i) beta cell viability and proliferation, (ii) basal and glucose-stimulated insulin secretion and (iii) canonical and non-canonical Wnt signalling pathways. We incubated rat INS-1E cells with 0.1, 1 or 5 μg/ml recombinant Sfrp5 for 24h. We measured basal and glucose-stimulated insulin secretion at glucose concentrations of 2.5 and 20 mmol/l. Phosphorylated and total protein content as well as mRNA levels of markers of cell proliferation, canonical and non-canonical Wnt signalling pathways were examined using Western blotting and real-time PCR. Differences between treatments were analysed by repeated measurement one-way ANOVA or Friedman's test followed by correction for multiple testing using the Benjamini-Hochberg procedure. At 5 μg/ml, Sfrp5 reduced mRNA levels of cyclin-B1 by 25% (p<0.05). At 1 and 5 μg/ml, Sfrp5 increased glucose-stimulated insulin secretion by 24% and by 34% (both p<0.05), respectively, but had no impact on basal insulin secretion. Sfrp5 reduced the phosphorylation of the splicing forms p46 and p54 of JNK by 39% (p<0.01) and 49% (p<0.05), respectively. In conclusion, Sfrp5 reduced markers of cell proliferation, but increased in parallel dose-dependently glucose-stimulated insulin secretion in INS-1E cells. This effect is likely mediated by reduced JNK activity, an important component of the non-canonical Wnt signalling pathway.

| S-EPMC6438539 | biostudies-literature

Interactome of Ca2+-bound secretagogin in INS-1E cells

Project description:By using His6-tagged recombinant human secretagogin in the presence of Ca2+ (100 µM), we precipitated putative interacting partners from INS-1E cells and identified their amino acid sequences by mass spectrometry. We detected canonical interacting proteins participating in vesicle-mediated transport, exocytosis and cytoskeletal organization. Besides, we captured proteins controlling protein folding and (de-)ubiquitination. Our data support that secretagogin modulates protein folding and degradation through protein-protein interactions and interacts with USP9X in β cells to control cell survival.

2017-06-21 | PXD006544 | Pride

Gene expression profile at single cell level of GFP labeled islet β cells from streptozotocin (STZ) treated Ins/β-lineage-labeled mice

Project description:Islet β cells suffer from de- and trans-differentiation after injury. We used single cell RNA sequencing (scRNA-seq) to analyze the diversity of β cells in from STZ-induced diabetes.

2023-05-01 | GSE203042 | GEO

Transcriptome profile of INS-1E Ctrl and DKO cells

Project description:To analyse gene expression differences between the TFEB/TFE3 KO cells vs. Controls, under growing conditions (GC) vs. Fasting conditions (Fast)

2023-07-31 | GSE153709 | GEO

FFA2-, but not FFA3-agonists inhibit GSIS of human pseudoislets: a comparative study with mouse islets and rat INS-1E cells.

Project description:The expression of short chain fatty acid receptors FFA2 and FFA3 in pancreatic islets raised interest in using them as drug targets for treating hyperglycemia in humans. This study aims to examine the efficacy of synthetic FFA2- and FFA3-ligands to modulate glucose-stimulated insulin secretion (GSIS) in human pseudoislets which display intact glucose responsiveness. The FFA2-agonists 4-CMTB and TUG-1375 inhibited GSIS, an effect reversed by the FFA2-antagonist CATPB. GSIS itself was not augmented by CATPB. The FFA3-agonists FHQC and 1-MCPC did not affect GSIS in human pseudoislets. For further drug evaluation we used mouse islets. The CATPB-sensitive inhibitory effect of 100 µM 4-CMTB on GSIS was recapitulated. The inhibition was partially sensitive to the Gi/o-protein inhibitor pertussis toxin. A previously described FFA2-dependent increase of GSIS was observed with lower concentrations of 4-CMTB (10 and 30 µM). The stimulatory effect of 4-CMTB on secretion was prevented by the Gq-protein inhibitor FR900359. As in human pseudoislets, in mouse islets relative mRNA levels were FFAR2 > FFAR3 and FFA3-agonists did not affect GSIS. The FFA3-agonists, however, inhibited GSIS in a pertussis toxin-sensitive manner in INS-1E cells and this correlated with relative mRNA levels of Ffar3 > > Ffar2. Thus, in humans, when FFA2-activation impedes GSIS, FFA2-antagonism may reduce glycemia.

| S-EPMC7536384 | biostudies-literature

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