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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Rapid, high efficiency isolation of pancreatic ß-cells

ABSTRACT: The ability to isolate pure pancreatic ß-cells would greatly aid multiple areas of diabetes research. We developed an exendin-4-like neopeptide conjugate for the rapid purification and isolation of functional pancreatic ß-cells. By targeting the glucagon-like peptide-1 receptor, ß-cells were isolated within an hour and were >99% pure. These studies were confirmed by immunostaining, confocal microscopy and microarray analysis on isolated cells. Gene expression profiling studies of the cytofluorometrically sorted ß-cells provided new insights into the genetic programs at play of different ages and stages during type-1 diabetes development. The described isolation method should have broad applicability to the ß-cell field. Microarray profile of beta cells from isolated islets from 4 and 12 week old NOD mice. Cells were stained with 50 nM Ex4+ probe and sorted on FACS ARIA. DAPI and CD45+ cells were excluded.

ORGANISM(S): Mus musculus

SUBMITTER: James Mohan

PROVIDER: E-GEOD-64508 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Rapid, high efficiency isolation of pancreatic ß-cells.

Clardy Susan M SM Mohan James F JF Vinegoni Claudio C Keliher Edmund J EJ Iwamoto Yoshiko Y Benoist Christophe C Mathis Diane D Weissleder Ralph R

Scientific reports 20150902

The ability to isolate pure pancreatic ß-cells would greatly aid multiple areas of diabetes research. We developed a fluorescent exendin-4-like neopeptide conjugate for the rapid purification and isolation of functional mouse pancreatic β-cells. By targeting the glucagon-like peptide-1 receptor with the fluorescent conjugate, β-cells could be quickly isolated by flow cytometry and were >99% insulin positive. These studies were confirmed by immunostaining, microscopy and gene expression profiling ...[more]

PMID: 26330153

Similar Datasets

Rapid, high efficiency isolation of pancreatic ß-cells

Project description:The ability to isolate pure pancreatic ß-cells would greatly aid multiple areas of diabetes research. We developed an exendin-4-like neopeptide conjugate for the rapid purification and isolation of functional pancreatic ß-cells. By targeting the glucagon-like peptide-1 receptor, ß-cells were isolated within an hour and were >99% pure. These studies were confirmed by immunostaining, confocal microscopy and microarray analysis on isolated cells. Gene expression profiling studies of the cytofluorometrically sorted ß-cells provided new insights into the genetic programs at play of different ages and stages during type-1 diabetes development. The described isolation method should have broad applicability to the ß-cell field.

2015-09-04 | GSE64508 | GEO

Argonaute2 mediates compensatory expansion of the pancreatic ß-cell

Project description:Pancreatic ß-cells adapt to compensate for the increased metabolic demand during insulin resistance. While the microRNA pathway has an essential role in the expansion of ß-cell mass, the extent of its contribution is unclear. Here we show that miR-184 is silenced in the pancreatic islets of several insulin-resistant mouse models and in the islets of type-2 diabetic human subjects. Reduction of miR-184 promotes the expression of its target Argonaute2 (Ago2), a component of the microRNA-induced silencing complex. While over-expression of Ago2 increased ß-cell proliferation, conditional deletion decreased ß-cell number. Moreover, restored expression of miR-184 in leptin-deficient ob/ob mice decreased Ago2 and prevented compensatory ß-cell expansion. Loss of Ago2 expression during insulin resistance blocked ß-cell growth and relieved the regulation of miR-375-targeted genes including the growth suppressor Cadm1. This study identifies the regulation of Ago2 by miR-184 as an essential component of the compensatory response to promote proliferation during insulin resistance.

2014-02-06 | GSE46623 | GEO

Mus musculus

Project description:Rapid, high efficiency isolation of pancreatic ß-cells

| PRJNA271154 | ENA

Stabilization of ß-catenin during murine Kidney Development

Project description:We define a pathogenic role for a ß-catenin-activated genetic pathway in murine renal dysplasia. Cre-mediated stabilization of ß-catenin in the ureteric cell lineage prior to the onset of kidney development increased ß-catenin levels and caused renal aplasia or severe hypodysplasia. A genome-wide analysis of mRNA expression in dysplastic tissue identified down-regulation of genes required for ureteric branching and up regulation of Tgfß2 and Dkk1. Hoxb7-Cre:EGFP mice ( Zhao, et al. (2004) Dev Biol 276:403-415) were crossed with mice containing loxP sites flanking exon 3 of the ß-catenin allele (ß-catdelta3/delta3) (Harada,et al. (2002) Cancer Res 62:1971-1977) to generate ß-catenin gain-of-function mutant mice specific to the uteric bud, termed ß-catGOF-UB .Eighteen ß-catGOF-UB mutant kidneys and 9 WT kidneys were micro-dissected at E12.5. Mutant kidneys were divided into three random pools (n=3) consisting of 6 kidneys each and mRNA expression assessed by microarray.

2011-03-28 | E-GEOD-20325 | biostudies-arrayexpress

Glucagon regulates Hepatic Kisspeptin1 to Impair Insulin Secretion in Diabetes Mellitus

Project description:Glucagon and insulin are counter-regulatory pancreatic hormones that precisely control blood glucose homeostasis1. Type 2 diabetes mellitus (T2DM) is characterized by inappropriately elevated blood glucagon2-5 levels as well as insufficient glucose stimulated insulin secretion (GSIS) by pancreatic ß-cells6. Early in the pathogenesis of T2DM, hyperglucagonemia is observable antecedent to ß-cell dysfunction7-9; and in mice, liver-specific activation of glucagon receptor-dependent signaling results in impaired GSIS10. However, the mechanistic relationship between hyperglucagonemia, hepatic glucagon action, and ß-cell dysfunction remains poorly understood. Here we show that glucagon action stimulates hepatic production of the neuropeptide kisspeptin1, which acts in an endocrine manner on ß-cells to suppress GSIS. In vivo glucagon administration acutely stimulates hepatic kisspeptin1 production, and kisspeptin1 is increased in livers from humans with T2DM and from mouse models of diabetes mellitus. Synthetic kisspeptin1 potently suppresses GSIS in vivo and in vitro from normal isolated islets, which express the kisspeptin1 receptor Kiss1R. Administration of a Kiss1R antagonist in diabetic Leprdb/db mice potently augments GSIS and reduces glycemia. Our observations indicate in the pathogenesis of T2DM an endocrine mechanism sequentially linking hyperglucagonemia via hepatic kisspeptin1 production to impaired insulin secretion. In addition, our findings suggest Kiss1R antagonism as a therapeutic avenue to improve ß-cell function in T2DM. Total RNA from L-Δprkar1a KO mice compared to control D-glucose mice

2014-04-01 | E-GEOD-48815 | biostudies-arrayexpress

Expression data from SOX9 overexpressing EndoC-ßH1 cells

Project description:Human ß cell dedifferentiation as a potent mechanism of diabetes is gaining prominence. Several data suggest an upregulation of the transcription factor SOX9, a progenitor and duct cell marker during ß cell dedifferentiation. However, its targets in such cells need more understanding. Here, we overexpressed SOX9 and a constitutively active mutant (VP16-SOX9∆TAD) in Human pancreatic beta EndoC-ßH1 cells in order to understand its targets.

2018-01-31 | GSE104195 | GEO

Intervention study of ß-hydroxy-ß-methyl butyric acid on sarcopenia in patients with colorectal cancer

Project description:Interventions: Experimental group:ß- hydroxy- ß- methyl butyrate;Control Group:No Primary outcome(s): skeletal muscle index;tumor necrosis factor-like weak apoptosis-inducing factor;peroxisome proliferator-activated receptor coactivator 1-a;growth differentiation factor 15;grip strength;pace;leg circumference Study Design: Parallel

| 2716507 | ecrin-mdr-crc

Glucagon regulates Hepatic Kisspeptin1 to Impair Insulin Secretion in Diabetes Mellitus

2014-04-01 | GSE48815 | GEO

Stabilization of ß-catenin during murine Kidney Development

2011-03-28 | GSE20325 | GEO

Expression data from Pseudomonas aeruginosa PAO1 and its isogenic ampR mutant in the presence and absence of sub-MIC ß-lactam exposure.

Project description:The transcriptional regulator AmpR controls expression of the AmpC ß-lactamase in P. aeruginosa and other bacteria. Studies have demonstrated that in addition to regulating ampC expression, AmpR also regulates the expression of the sigma factor AlgT/U and the production of some quorum-sensing regulated virulence factors. In order to understand the ampR regulon, we compared the expression profiles of PAO1 and its isogenic ampR mutant, PAO∆ampR in the presence and absence of sub-MIC ß-lactam stress. The analysis demonstrates that the ampR regulon is much more extensive than previously thought, with the deletion of ampR affecting the expression of over 300 genes. Expression of an additional 207 genes are affected by AmpR when the cells are exposed to sub-MIC ß-lactam stress, indicating that the ampR regulon in P. aeruginosa is much more extensive than previously thought. An inframe deletion of ampR was generated in P. aeruginosa PAO1. The wild type and ampR mutant strains were grown to mid-log phase and subjected to sub-MIC ß-lactam exposure. Total RNA was isolated from 2-hour ß-lactam exposed and unexposed cells to monitor changes in gene expression arising due to loss of ampR in the presence and absence of ß-lactam exposure.

2012-03-29 | E-GEOD-33188 | biostudies-arrayexpress

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