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Transcription profiling of mouse MIN6 insulinoma beta cells following knock-down of murine Pdx1

ABSTRACT: In order to identify genes that are regulated by Pdx1, MIN6 insulinoma cells were transduced with adenovirus expressing a short hairpin RNA directed against murine Pdx1 (AdshPdx1) or luciferase (AdshLuc) or not transduced at all (untreated). RNA was harvested and reverse transcribed. Reduced expression of Pdx1 and established Pdx1 targets was confirmed. The RNA was then submitted for labeling and hybridization to the PancChip cDNA microarray.

ORGANISM(S): Mus musculus

SUBMITTER: David Groff

PROVIDER: E-MTAB-132 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Pdx1 (MODY4) regulates pancreatic beta cell susceptibility to ER stress.

Sachdeva Mira M MM Claiborn Kathryn C KC Khoo Cynthia C Yang Juxiang J Groff David N DN Mirmira Raghavendra G RG Stoffers Doris A DA

Proceedings of the National Academy of Sciences of the United States of America 20091023 45

Type 2 diabetes mellitus (T2DM) results from pancreatic beta cell failure in the setting of insulin resistance. Heterozygous mutations in the gene encoding the beta cell transcription factor pancreatic duodenal homeobox 1 (Pdx1) are associated with both T2DM and maturity onset diabetes of the young (MODY4), and low levels of Pdx1 accompany beta cell dysfunction in experimental models of glucotoxicity and diabetes. Here, we find that Pdx1 is required for compensatory beta cell mass expansion in r ...[more]

PMID: 19855005

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Transcription profiling of the islets from Pdx1+/- mice compared to islets isolated from Pdx1 +/+ littermates

Project description:The aim of this experiment was to use global gene expression profiling to identify genes that are differentially expressed in the islets from Pdx1+/- mice compared to islets isolated from Pdx1 +/+ littermates. The Pdx1 null mutation consists of a nuclear targeted _-galactosidase cassette fused in-frame with the N terminus of PDX-1.

2009-12-02 | E-MTAB-127 | biostudies-arrayexpress

Selenomethionine modulates insulin secretion in the MIN6-K8 mouse insulinoma cell line.

Project description:Selenium is an essential trace element of interest for its potential role in glucose homeostasis. The present study investigated the impact of selenium supplementation as selenomethionine (SeMet) on insulin secretion in MIN6-K8 cells, a pancreatic β-cell model. We found that SeMet enhanced percent glucose-induced insulin secretion, while also increasing tolbutamide- and KCl-induced percent insulin secretion. RNA-sequencing showed that SeMet supplementation altered expression of several selenoproteins, including glutathione peroxidase 3 (Gpx3) and selenoprotein P (SelP). Targeted knockdown of Gpx3 increased both percent and total insulin release, while SelP knockdown increased insulin content and insulin release. Collectively, these studies support a putative role for selenium and selenoproteins in the regulation of insulin secretion, glucose homeostasis, and diabetes risk.

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Exendin-4 treatment of Pancreatic Islets

Project description:The aim of the study was to investigate the effect of Exendin-4 on isolated pancreatic islets allowing for the elucidation of the various transcriptional programs initiated by this multifunctional peptide hormone. Islets were treated with Exendin-4 for 30 and 180 minutes. After these time points, RNA was isolated and used for hybridization against matched control islets using the Mouse PancChip 6.

2014-11-13 | E-MTAB-3117 | biostudies-arrayexpress

Metabolomic identification of biochemical changes induced by fluoxetine in an insulinoma cell line (MIN6).

Project description:Background and purposeThe use of fluoxetine raises the risk of pancreatic beta-cell dysfunction. However, the specific mechanism behind its mechanism of action in beta cells is unknown. This study investigated the cellular response of MIN6 cells to fluoxetine using untargeted cell-based metabolomics.Experimental approachMetabolic profiling of MIN6 cells was performed using liquid chromatography-high resolution mass spectrometry (LC-HRMS) analysis on samples prepared under optimized conditions, followed by principal component analysis, partial least squares-discriminant analysis, and pair-wise orthogonal projections to latent structures discriminant analyses.Findings/resultsSixty-six metabolites that had been differentially expressed between the control and fluoxetine-treated groups demonstrated that the citric acid cycle is mainly perturbed by fluoxetine treatment.Conclusion and implicationsThe current study provides insights into the molecular mechanisms of fluoxetine effects in MIN6 cells.

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Identification of Sox9/Pdx1-coregulated Genes During Pancreas Organogenesis

Project description:Sox9/Pdx1 co-regulated target genes were identified by comparing gene expression in Sox9/Pdx1-double heterozygates versus Sox9- or Pdx1- heterozygates pancreata using microarray analysis. Pdx1LacZko (herein designated Pdx1-/+) (Offield et al. 1996) and one Sox9 allele was conditionally deleted in the developing pancreas via recombination of a Sox9-flox allele (Kist et al., 2002) using the Foxa3-Cre transgene (Lee et al., 2005). Total RNA was isolated and pooled from dorsal pancreatic epithelia of e12.5 Sox9fl/+; Foxa3-Cre (Sox9 het), Pdx1-/+ (Pdx1 het) versus Sox9fl/+; Foxa3-Cre; Pdx1-/+ (Sox9/Pdx1 double hets) littermates for three biological replicates

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Glucocorticoids differentially regulate the expression of CRFR1 and CRFR2? in MIN6 insulinoma cells and rodent islets.

Project description:Urocortin 3 (Ucn 3), member of the corticotropin-releasing factor (CRF) family of peptide hormones, is released from ?-cells to potentiate insulin secretion. Ucn 3 activates the CRF type-2 receptor (CRFR2) but does not activate the type-1 receptor (CRFR1), which was recently demonstrated on ?-cells. While the direct actions of Ucn 3 on insulin secretion suggest the presence of cognate receptors within the islet microenvironment, this has not been established. Here we demonstrate that CRFR2? is expressed by MIN6 insulinoma cells and by primary mouse and human islets, with no detectable expression of CRFR2?. Furthermore, stimulation of MIN6 cells or primary mouse islets in vitro or in vivo with glucocorticoids (GCs) robustly and dose-dependently increases the expression of CRFR2?, while simultaneously inhibiting the expression of CRFR1 and incretin receptors. Luciferase reporters driven by the mouse CRFR1 or CRFR2? promoter in MIN6 cells confirm these differential effects of GCs. In contrast, GCs inhibit CRFR2? promoter activity in HEK293 cells and inhibit the expression of CRFR2? in A7r5 rat aortic smooth muscle cells and differentiated C2C12 myotubes. These findings suggest that the GC-mediated increase of CRFR2? depends on the cellular context of the islet and deviates from the GC-mediated suppression of CRFR1 and incretin receptors. Furthermore, GC-induced increases in CRFR2? expression coincide with increased Ucn 3-dependent activation of cAMP and MAPK pathways. We postulate that differential effect of GCs on the expression of CRFR1 and CRFR2? in the endocrine pancreas represent a mechanism to shift sensitivity from CRFR1 to CRFR2 ligands.

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Chromatin immunoprecipitation of mouse MIN6 pancreatic beta cells to identify Pdx1 targets

Project description:The aim of this experiment was to use highthroughput chromatin immunoprecipitation followed by hybridization to promoter microarrays to obtain a comprehensive list of sites in the genome that are physically occupied by Pdx1. Chromatin was prepared from Min6 insulinoma cells and immunoprecipitated with Pdx1 or control antiserum. The precipitated chromatin was then purified, amplified and directly sequenced using Illumina technology.

2009-12-02 | E-MTAB-134 | biostudies-arrayexpress

Microarray Analysis of MIN6 cells treated with Exendin-4 over time

Project description:The aim of the study was to investigate the effect of Exendin-4 on MIN6 cells allowing for the elucidation of the various transcriptional programs initiated by this multifunctional peptide hormone. MIN6 cells were treated with Exendin-4 for 24, 48 and 72 hours. After these time points RNA was isolated and used for hybridization (on Cy3) against matched control MIN6 cells (on Cy5) using the Mouse PancChip 5.0 . Three assays were carried out for each time point.

2014-11-04 | E-MTAB-3071 | biostudies-arrayexpress

Evaluation of Viburnum opulus L. Fruit Phenolics Cytoprotective Potential on Insulinoma MIN6 Cells Relevant for Diabetes Mellitus and Obesity.

Project description:In this study, the influence of guelder rose (Viburnum opulus) fruit fresh juice (FJ) and a phenolic-rich fraction (PRF) isolated from juice on mice insulinoma MIN6 cells activities was investigated. Extracts were able to decrease intracellular oxidative stress at the highest non-cytotoxic concentrations. They induced glucagon-like peptide-1 (GLP-1) secretion in the presence of an elevated glucose concentration, and they inhibited in vitro activity of the dipeptidyl peptidase-4 (DPP4) enzyme. Nonetheless, inhibition of glucose-stimulated insulin secretion was detected, which was accompanied by a decrease of cellular membrane fluidity and hyperpolarization effect. In addition, the increase of free fatty acid uptake and accumulation of lipid droplets in MIN6 cells were observed. Elevated extract concentrations induced cell apoptosis through the intrinsic mitochondrial pathway with activation of initiatory caspase-9 and downstream caspases-3/7. The fluorescence-quenching studies indicated that PRF extract has binding affinity to human serum albumin, which is one of the factors determining drug bioavailability. Taken together, despite the cytoprotective activity against generated intracellular oxidative stress, V. opulus revealed potential toxic effects as well as decreased insulin secretion from MIN6 cells. These findings are relevant in understanding V. opulus limitations in developing diet supplements designed for the prevention and treatment of postprandial glucose elevation.

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Selenomethionine Modulates Insulin Secretion in the MIN6-K8 Mouse Insulinoma Cell Line

Project description:Selenium is an essential trace element that has gained interest for its potential role in glucose homeostasis. The purpose of the present study was to investigate the impact of selenium supplementation as selenomethionine (SeMet) on insulin secretion in MIN6-K8 cells, a model of pancreatic -cells. We found that 40 μM and 80 μM SeMet significantly enhanced percent insulin secretion at low (2.8 mM), intermediate (11.7 mM), and high (16.7 mM) glucose stimulation. SeMet also increased tolbutamide- or KCl-induced percent insulin secretion at 40 μM and 80 μM. Ca2+ influx was only reduced with 80 μM SeMet. RNA-sequencing showed that 40 μM SeMet supplementation upregulated expression of selenoprotein H (SelH) and thioredoxin reductase 1 (Txnrd 1) and downregulated expression of glutathione peroxidase 3 (Gpx3), selenoprotein O (SelO), and selenoprotein P (SelP). Gpx3 knockdown increased both percent and total insulin release with high glucose stimulation. SelP knockdown increased insulin release at high glucose. In conclusion, high SeMet supplementation augments insulin secretion, while reductions in Gpx3 and SelP expression, from SeMet supplementation or via silencing, augment -cell function in the MIN6-K8 cell line. These studies support a putative role for selenium and selenoproteins in the regulation of glucose homeostasis and diabetes risk.

2024-03-13 | GSE183775 | GEO

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