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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.

ORGANISM(S): Mus musculus

PROVIDER: GSE64508 | GEO | 2015/09/04

SECONDARY ACCESSION(S): PRJNA271154

REPOSITORIES: GEO

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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. 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.

2015-09-04 | E-GEOD-64508 | biostudies-arrayexpress

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

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

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

2014-04-01 | GSE48815 | GEO

Transient ER stress cell-autonomously promotes beta cell cycling

Project description:Regenerating endogenous pancreatic ß-cells is a potentially curative yet currently elusive strategy for diabetes therapy. Mimicking the microenvironment of the developing pancreas and leveraging vascular signals that support pancreatic endocrinogenesis may promote ß-cell regeneration. We aimed to investigate whether recovery from experimental hypovascularization of the endocrine pancreas, achieved by modulating the transgenic production of a VEGF-A blocker in ß-cells, could trigger mouse ß-cell proliferation. Serendipitously, we found that transgene overexpression in ß-cells induces endoplasmic reticulum (ER) stress and that subsequent relief from this stress stimulates ß-cell proliferation independent of vessel recovery. Transient GFP overexpression in vivo and transient chemical induction of ER stress in vitro replicated this ß-cell cycling response. Our findings highlight the potential side effects of ER stress due to transgene overexpression in ß-cells and assert that ER stress relief serves as a potent regenerative stimulus.

2025-12-19 | GSE274443 | GEO

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

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

Effect of lncMGC on gene expression of kidney mesangial cells under SD or TGF-ß treatment [ATAC-seq]

Project description:To investigate the function of long noncoding RNA lncMGC in WT and lncMGC KO mouse kidney mesangial cells treated with TGF-ß. Assay for Transposase-Accessible Chromatin (ATAC) sequencing on 4 types of kidney messangial cell samples: isolated from wild type (WT) or lncMGC knockout (lncMGC_KO) mouses, each treated with either SD or TGF-ß, namely WT_SD, WT_TGF, KO_SD and KO_TGF.

2023-06-21 | GSE229686 | GEO

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