Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcription profiling of mouse islet growth after partial pancreatectomy and exendin-4 Treatment

ABSTRACT: Diabetes mellitus results from an inadequately functioning beta-cell mass. In the adult pancreas, beta-cell mass is dynamic, increasing to meet metabolic demands and decreasing with metabolic or injury insults. Exendin-4 (Ex-4) is a glucagon-like peptide-1 receptor agonist that augments beta-cell mass by increasing beta-cell neogenesis and proliferation and by reducing apoptosis. We utilized a cDNA microarray approach to identify genes that are differentially regulated during islet growth after Ex-4 treatment or a partial pancreatectomy (Ppx). Mice underwent 50% Ppx or sham operation and received Ex-4 or vehicle every 24 hours. cDNA prepared from total pancreatic RNA isolated at 12, 24 and 48 hrs after surgery was hybridized to the PancChip 4.0 microarray.

ORGANISM(S): Mus musculus

SUBMITTER: Doris Stoffers

PROVIDER: E-CBIL-5 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Identification of transcriptional targets during pancreatic growth after partial pancreatectomy and exendin-4 treatment.

De León Diva D DD Farzad Cyrus C Crutchlow Michael F MF Brestelli John J Tobias John J Kaestner Klaus H KH Stoffers Doris A DA

Physiological genomics 20060101 2

After partial pancreatectomy (Ppx), substantial regeneration of the endocrine and exocrine pancreatic compartments has been shown in adult rodents. Exendin-4 (Ex-4) is a glucagon-like peptide-1 receptor agonist that augments endocrine beta-cell mass by stimulating neogenesis, proliferation, and cell survival. After Ppx, treatment with Ex-4 ameliorates hyperglycemia by stimulating beta-cell mass recovery. We utilized a cDNA microarray approach to identify genes differentially regulated during pan ...[more]

PMID: 16410542

Similar Datasets

Cytotoxicity Study of Rat INS1 cell lines

Project description:Cytokines IL-1 and IFN-gamma have been shown to be the primary effectors of beta-cell destruction during the immune response. The aim of this study was to identify the gene expression changes that are associated with resistance of beta cells to cytokines. INS-1 rat insulinoma cells were grown in increasing doses of cytokines until a resistance phenotype had developed. RNA was prepared from these cytokine resistant sublines as well as the original, cytokine-sensitive parental INS-1 cells in Dr. Chris Newgard's lab, quantified and sent frozen in water. 3-7 biological replicates per condition were sent for the following three conditions: (i) 834/40, Cytokine-sensitive (CS), (ii) 833/15 and 833/117, Cytokine resistant grown in the absence of cytokines (CRu), (iii) 833/15C and 833/117C: Cytokine Resistant Grown in the Presence of Cytokines (CRt)

2014-07-22 | E-MTAB-2776 | biostudies-arrayexpress

Gene expression profiling of MafA, MafB, and MafA/MafB Mutants in E18.5 pancreas

Project description:MafA and MafB transcription factors have been shown to be key regulators of insulin and glucagon transcription. MafB is essential for alpha and beta cell differentiation, as MafB deficient mice produced fewer insulin+ and glucagon+ cells during development, with MafA expressed in remaining insulin+ cells. In contrast, beta cell development was reported to be normal in a total MafA knock out, although the animals developed beta cell dysfunction and diabetes as adults. However, we have found that MafB expression is elevated during development and retained in adult insulin+ cells after conditional removal of MafA in the pancreas. These studies will evaluate the broader significance of these insulin and glucagon regulators in alpha and beta cell development and function. Our efforts will focus on determining if the concerted actions of MafA and MafB factors are significant to beta cell formation, and we specifically plan to: Determine how alpha and beta cell differentiation is affected in MafA/MafB compound mutant mice during pancreas development. cDNA microarray studies (pancchip 6.0) with wild type, MafAKO, MafB-/-, and MafAKOMafB-/- mutant E18.5 pancreata will be performed to comprehensively identify genes controlled by MafA and MafB in developing alpha and beta cells.

2014-11-04 | E-MTAB-3070 | biostudies-arrayexpress

Transcription profiling of wild type and Foxa2 knock out mouse mature beta cells

Project description:The winged helix transcription factor Foxa2 regulates Pdx1 gene expression and fetal endocrine pancreas development. We show here by inducible gene ablation that Foxa2 inactivation in mature beta-cells induces hyperinsulinemic hypoglycemia in Foxa2loxP/loxP, Pdx1-CreERT2 adult mice. Mutant beta-cells exhibited a markedly increased pool of docked insulin granules, some of which were engaged in sequential or compound exocytosis, consistent with an increased first phase glucose-stimulated insulin secretion. Expression of multiple genes involved in vesicular trafficking, membrane targeting and fuel-secretion pathways is dependent on Foxa2. In addition, impaired cytosolic Ca2+ oscillations and elevated intracellular cAMP production accompanied this secretory defect, and were likely contributors to the sensitization of the exocytotic machinery. Thus, in the absence of Foxa2, alterations in intracellular second messenger signaling redistribute the insulin granules into the readily releasable pool. We conclude that Foxa2 is required both for the fetal pancreas development and for the function of mature beta-cells.

2007-09-22 | E-CBIL-39 | biostudies-arrayexpress

Transcription profiling of Foxa2 knock-outs in mice to better define the role of this gene in glucose homeostasis

Project description:Study to further characterize the genetic and functional consequence of the beta cell-specific ablation of Foxa2 (hepatocyte nuclear factor 3 beta, HNF-3b) in mice to better define the role of this gene in glucose homeostasis. The study involved 8 two-channel assays on UPenn Mouse PancChip 4.0, each consisting of a competitive mutant vs control hybridization. 4 control and 4 Foxa2loxP/loxP;Ins.CRE RNA samples were hybridized to the array using a dye-swap design. (The results from one of these assays had to be discarded from the analyses, so 7 assays were used.)

2006-06-30 | E-CBIL-13 | biostudies-arrayexpress

The role of Raf-1 kinase inhibitor protein in the regulation of pancreatic beta cell proliferation in mice

Project description:AIMS/HYPOTHESIS: Manoeuvres aimed at increasing beta cell mass have been proposed as regenerative medicine strategies for diabetes treatment. Raf-1 kinase inhibitor protein 1 (RKIP1) is a common regulatory node of the mitogen-activated protein kinase (MAPK) and nuclear factor κB (NF-κB) pathways and therefore may be involved in regulation of beta cell homeostasis. The aim of this study was to investigate the involvement of RKIP1 in the control of beta cell mass and function. METHODS: Rkip1 (also known as Pebp1) knockout (Rkip1 (-/-)) mice were characterised in terms of pancreatic and glucose homeostasis, including morphological and functional analysis. Glucose tolerance and insulin sensitivity were examined, followed by assessment of glucose-induced insulin secretion in isolated islets and beta cell mass quantification through morphometry. Further characterisation included determination of endocrine and exocrine proliferation, apoptosis, MAPK activation and whole genome gene expression assays. Capacity to reverse a diabetic phenotype was assessed in adult Rkip1 (-/-) mice after streptozotocin treatment. RESULTS: Rkip1 (-/-) mice exhibit a moderately larger pancreas and increased beta cell mass and pancreatic insulin content, which correlate with an overall improvement in whole body glucose tolerance. This phenotype is established in young postnatal stages and involves enhanced cellular proliferation without significant alterations in cell death. Importantly, adult Rkip1 (-/-) mice exhibit rapid reversal of streptozotocin-induced diabetes compared with control mice. CONCLUSIONS/INTERPRETATION: These data implicate RKIP1 in the regulation of pancreatic growth and beta cell expansion, thus revealing RKIP1 as a potential pharmacological target to promote beta cell regeneration. Pancreatic gene expression of Rkip-1 (Raf kinase inhibitor 1) knockout (KO) and wild type (WT) mice, including three biological replicates in each group.

2012-11-19 | E-GEOD-31150 | biostudies-arrayexpress

Transcription profiling of HNF4 alpha null mice to investigate the phenotype of dis-regulated insulin secretion and abnormal beta cell growth

Project description:The aim of this experiment was to use microarray analysis to examine the phenotype of dis-regulated insulin secretion and abnormal beta cell growth in HNF4 alpha null mice. These mice show impaired glucose tolerance and elevated fasting and fed plasma insulin levels. Rana Gupta from Klaus Kaestner's Lab extracted RNA from isolated islets. Three controls and five mutants were provided for the study.

2006-09-05 | E-CBIL-6 | biostudies-arrayexpress

Chromatin immunoprecipitation and transcription of mouse liver in the presence or absence of exogenous glucocorticoid to identify direct targets of the glucocorticoid receptor

Project description:The purpose of this study was to identify direct targets of the glucocorticoid receptor (GR) using an orthogonal analysis. An expression study of mouse livers in the presence or absence of exogenous glucocorticoid complemented a genome-wide location analysis on chromatin from the same livers. These were hybridized to the BCBC Mouse PancChip 5.0 and the Mouse PromoterChip BCBC-3.0 respectively.

2007-09-14 | E-CBIL-38 | biostudies-arrayexpress

Chromatin immunoprecipitation of wild type and Foxa2 knock-out mouse liver using anti-HNF6 anitbodies to test whether Foxa2 inhibits HNF6-mediated transcription in the liver

Project description:The aim of this study was to test, in vivo, if Foxa2 inhibits HNF6-mediated transcription in the liver. We utilized hepatocyte-specific gene ablation of Foxa2 and the Mouse PromoterChip BCBC 3.0 and Mouse PancChip 5.0 cDNA microarrays to investigate HNF6 binding to its target promoters in vivo in the presence or absence of Foxa2. For the mouse promoter microarray analysis, chromatin immunoprecipitation using anti-HNF6 antibodies was performed on chromatin isolated from Foxa2loxP/loxP Alfp.Cre and control mouse livers. Along with sheared genomic DNA (common reference), the immunoprecipitated DNA was amplified, labeled and hybridized to the Mouse PromoterChip BCBC 3.0. For microarray analysis of gene expression, liver RNAs were isolated from three Foxa2loxP/loxP Alfp.Cre and three control mice. RNAs were reverse transcribed, labeled, and hybridized to the Mouse PancChip 5.0. Overall, our studies demonstrate that HNF6 binds to and regulates its target promoters in vivo in the presence and absence of Foxa2 and that the expression levels of HNF6 targets are not influenced by Foxa2.

2007-09-14 | E-CBIL-36 | biostudies-arrayexpress

Transcription profiling of wild type and C/EBPbeta deficient mice during a partial hepatectomy time series to identify transcriptional targets of C/EBPbeta

Project description:The aim of this experiment was to use microarray analysis to compare the response of wild type (WT) and C/EBPbeta deficient (KO) mice during a partial hepatectomy time course in hopes of identifying transcriptional targets of C/EBPbeta. In addition, the WT time course alone was examined to analyze mammalian cellular proliferation in vivo. In the partial hepatectomy model, quiescent hepatocytes reenter the cell cycle and progress in a synchronous fashion. This allows for the elucidation of regulatory networks operative in mammalian cell cycle. (Identification of transcriptional networks during liver regeneration (2004) Journal of Biological Chemistry)

2006-10-03 | E-CBIL-16 | biostudies-arrayexpress

Transcription profiling of rat insulinoma (INS-1 derived) cell lines that vary in their glucose responsiveness

Project description:The aim of this study was to identify the gene expression changes associated with glucose responsiveness in Rat INS-1 derived cell lines. RNA was prepared from cell lines which were shown to be highly glucose responsive and also lines which were shown to be poorly glucose responsive. Dr. Chris Newgard's lab quantified the RNA and sent it frozen in water. 3 biological replicates per condition were sent for the following conditions: (i) 832/13 and 833/15, robust glucose responsiveness; (ii)832/1 and 832/2 showed poor glucose responsiveness.

2007-09-11 | E-CBIL-35 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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