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

ABSTRACT: 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.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE53453 | GEO | 2013/12/19

SECONDARY ACCESSION(S): PRJNA232041

REPOSITORIES: GEO

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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

Human islets exposed to cytokines IL-1β and IFN-γ

2013-12-19 | GSE53454 | GEO

Human islets 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. Human islets were isolated and exposed (or not) to IL-1β and IFN-γ. The samples were collected at various time points for profiling with Affymetrix arrays. These measurements were performed three times.

2013-12-19 | E-GEOD-53454 | biostudies-arrayexpress

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

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

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

ImmGen Cytokines: Interferons

Project description:ImmGen Cytokines: Interferons

| PRJNA303161 | ENA

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

ImmGen cytokines: Signatures of “common γ-chain” family cytokines

Project description:ImmGen cytokines: Signatures of “common γ-chain” family cytokines

| PRJNA746283 | ENA

Role of cytokines in cardiac fibrosis and exercise

Project description:During acute sympathetic stress, the overeactivation of β-adrenergic receptors (β-ARs) caused cardiac fibrosis, by triggering inflammation and cytokine expression. It is unknown whether exercise training inhibited acute β-AR overactivation-induced cytokine expression and cardiac injury. Here, we reported that running exercise inhibited cardiac fibrosis and improved cardiac function in mice treated by isoproterenol, a β-AR agonist. Cytokine antibody array revealed that exercise prevented the expression changes of most cytokines induced by isoproterenol. Specifically, 18 ISO-upregulated and 3 ISO-downregulated cytokines belonged to six families (eg. chemokine) were prevented. A further KEGG analysis of these cytokines revealed that Hedgehog and Rap1 signaling pathways were involved in the regulation of cytokine expression by exercise. The expression changes of some cytokines that were prevented by exercise were verified by ELISA and real-time PCR. In conclusion, running exercise prevented the cytokine changes following acute β-AR overactivation and therefore attenuated cardiac fibrosis.

2019-03-30 | GSE129022 | GEO

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