U.S. flag

An official website of the United States government

Format
Items per page
Sort by

Send to:

Choose Destination

Links from GEO DataSets

Items: 20

1.

Modeling pancreatic beta cell senescence by induction of DNA double-strand breaks

(Submitter supplied) Pancreatic beta cell senescence occurs during the development of Type 1 Diabetes. To model the transcriptional responses of islet cells to DNA damage, we previously developed a human islet culture model in which the DNA damage response and senescence can be induced via double strand-breaks with the agent bleomycin. Here, we report the transcriptome-wide changes in human pancreatic islet cells following bleomycin exposure.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
12 Samples
Download data: XLSX
2.

Characterization of EndoC-BH5 a novel human pancreatic beta cell line

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
16 Samples
Download data
Series
Accession:
GSE224732
ID:
200224732
3.

Characterization of EndoC-BH5 a novel human pancreatic beta cell line. Comparative expression profile after stimulation stimulation with Interferon gamma and interleukin 1b.

(Submitter supplied) Responsiveness of EndoC-BH5 cells to cytokines was examined by RNA-seq of cells treated with IFNγ and IL1β for 24 h. The treatment resulted in profound changes in their transcriptome and upregulation of genes involved in the inflammatory pathwayand antigen processing and presentation, similar to previous studies on EndoC-BH1 cells and adult human islets. EndoC-BH5 cells hence represent a powerful tool to investigate the dialogue between beta cells and the immune system.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
6 Samples
Download data: TXT
Series
Accession:
GSE224731
ID:
200224731
4.

Characterization of EndoC-BH5 a novel human pancreatic beta cell line. Comparative expression profile with EndoC-BH1 and effect of stimulation with Interferon gamma and interleukin 1b.

(Submitter supplied) We have developped a novel human pancreatic beta cell line: EndoC-βH5. EndoC-βH5 cells are ready-to-use and storable cells with physiological insulin secretion. EndoC-βH5 cells were generated by integrative gene transfer of immortalizing transgenes hTERT and SV40 large T along with Herpes Simplex Virus-1 thymidine kinase into human fetal pancreas. Immortalizing transgenes were removed after amplification using CRE activation and remaining non-excized cells eliminated using ganciclovir. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
10 Samples
Download data: TXT
Series
Accession:
GSE224660
ID:
200224660
5.

Targeted elimination of senescent beta cells prevents Type 1 Diabetes

(Submitter supplied) scRNA-seq of Islets isolated from 8, 14 and 16 week NOD mice
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
9 Samples
Download data: MTX, TSV
Series
Accession:
GSE117770
ID:
200117770
6.

Unique human beta-cell senescence-associated secretory phenotype (SASP) reveal conserved signaling pathways and heterogeneous factors

(Submitter supplied) The aging of pancreatic beta-cells may undermine their ability to compensate for insulin resistance, leading to the development of type 2 diabetes (T2D). Aging beta-cells acquire markers of cellular senescence and develop a senescence-associated secretory phenotype (SASP) that can lead to senescence and dysfunction of neighboring cells through paracrine actions, contributing to beta-cell failure. Herein, we defined the beta-cell SASP signature based on unbiased proteomic analysis of conditioned media of cells obtained from human senescent beta-cells. more...
Organism:
Homo sapiens
Type:
Protein profiling by protein array
Platform:
GPL28516
27 Samples
Download data: DATA
Series
Accession:
GSE162521
ID:
200162521
7.

SASP signature of beta-cells includes pro-inflammatory and stress response proteins

(Submitter supplied) To define the senescence-associated secretory phenotype (SASP) of beta-cells, we used conditioned media (CM) generated from bleomycin-treated MIN6 cells and from senescent (beta-Gal-positive) primary beta-cells. In order to culture senescent beta-cells, we isolated islet, FACS-sorted them into beta-Gal-positive and negative populations, excluding immune cells through negative selection of CD45-positive and CD11beta-positive cells. more...
Organism:
Mus musculus; Homo sapiens
Type:
Protein profiling by protein array
Platform:
GPL28516
28 Samples
Download data: TXT
Series
Accession:
GSE150285
ID:
200150285
8.

Senescent beta-cells exhibit a unique secretory phenotype that promotes inflammation and remodeling of the extracellular environment

(Submitter supplied) Type 2 Diabetes (T2D) patients have higher proportions of senescent beta-cells than their non-diabetic counterparts (Aguayo-Mazzucato et al., 2019). Senescent beta-cells may propagate dysfunction in neighboring cells through the paracrine effects of the senescence-associated secretory phenotype (SASP). To address the heterogeneity in beta-cell SASP expression and its role in T2D, we measured expression levels of beta-cell SASP signature genes in a mouse model of acute insulin resistance using the insulin receptor antagonist, S961. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
3 Samples
Download data: CSV
Series
Accession:
GSE149984
ID:
200149984
9.

Decreased IGF1R Attenuates Senescence and Improves Function in Pancreatic beta-Cells

(Submitter supplied) We previously reported that increased expression of IGF1R in mouse and human beta-cells is a marker of older beta-cells; however, its contribution to age-related dysfunction and cellular senescence remains to be determined. In this study, we explored the direct role of IGF1R in beta-cell function and senescence using inducible beta-cell specific IGF1R knockdown (betaIgf1rKD) mice. Adult betaIgf1rKD mice showed improved glucose clearance and glucose-induced insulin secretion, accompanied by decreased p21Cip1 protein expression in beta-cells. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
8 Samples
Download data: CSV
Series
Accession:
GSE229709
ID:
200229709
10.

Epigenetic modulation of β-cells by interferon-α via PNPT11-miR-26a-TET2 triggers autoimmune diabetes

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Methylation profiling by genome tiling array; Expression profiling by high throughput sequencing
Platforms:
GPL13534 GPL11154
12 Samples
Download data: TXT
Series
Accession:
GSE124811
ID:
200124811
11.

Epigenetic modulation of β-cells by interferon-α via PNPT11-miR-26a-TET2 triggers autoimmune diabetes [RNA-seq]

(Submitter supplied) Type 1 diabetes (T1D) is caused by autoimmune destruction of pancreatic β cells. Mounting evidence supports a central role for β-cell alterations in triggering the activation of self-reactive T-cells in T1D. However, the early deleterious events that occur in β cells, underpinning islet autoimmunity are not known. We hypothesized that epigenetic modifications induced in β cells by inflammatory mediators play a key role in initiating the autoimmune response. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
6 Samples
Download data: TXT
12.

Epigenetic modulation of β-cells by interferon-α via PNPT11-miR-26a-TET2 triggers autoimmune diabetes [methylation array]

(Submitter supplied) Type 1 diabetes (T1D) is caused by autoimmune destruction of pancreatic β cells. Mounting evidence supports a central role for β-cell alterations in triggering the activation of self-reactive T-cells in T1D. However, the early deleterious events that occur in β cells, underpinning islet autoimmunity are not known. We hypothesized that epigenetic modifications induced in β cells by inflammatory mediators play a key role in initiating the autoimmune response. more...
Organism:
Homo sapiens
Type:
Methylation profiling by genome tiling array
Platform:
GPL13534
6 Samples
Download data: TXT
Series
Accession:
GSE124809
ID:
200124809
13.

Characterisation of the functional and transcriptomic effects of pro-inflammatory cytokines on human EndoC-βH5 beta cells

(Submitter supplied) EndoC-βH5 is a newly established human beta-cell model which may be superior to previous models of native human beta cells. Exposure of beta cells to proinflammatory cytokines is a widely used in vitro model of immune-mediated beta-cell failure in type 1 diabetes and we therefore performed an in-depth characterisation of the effects of cytokines on EndoC-βH5 cells. Global gene expression was characterised by stranded RNA sequencing.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL28038
8 Samples
Download data: TXT
Series
Accession:
GSE218735
ID:
200218735
14.

Inhibition of 12/15-Lipoxygenase Protects Against β Cell Oxidative Stress and Glycemic Deterioration in Mouse Models of Type 1 Diabetes

(Submitter supplied) Islet β-cell dysfunction and aggressive macrophage activity are early features in the pathogenesis of type 1 diabetes (T1D). 12/15-lipoxygenase (12/15-LOX) is induced in β cells and macrophages during T1D and produces pro-inflammatory lipids and lipid peroxides that exacerbate β-cell dysfunction and macrophage activity. Inhibition of 12/15-LOX provides a potential therapeutic approach to prevent glycemic deterioration in T1D. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
12 Samples
Download data: CSV
Series
Accession:
GSE101722
ID:
200101722
15.

PAHSAs reduce cellular senescence and protect pancreatic beta cells from metabolic stress through regulation of Mdm2/p53

(Submitter supplied) Senescence in pancreatic beta cells plays a major role in beta cell dysfunction which leads to impaired glucose homeostasis and diabetes. Therefore, prevention of beta cell senescence could reduce the risk of diabetes. Treatment of NOD mice, a model of Type 1 autoimmune diabetes (T1D), with Palmitic acid hydroxy stearic acids (PAHSAs), a novel class of endogenous lipids with antidiabetic and anti-inflammatory effects, delays the onset and reduces the incidence of T1D from 82% with vehicle treatment to 35% with PAHSAs. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
8 Samples
Download data: CSV
Series
Accession:
GSE216051
ID:
200216051
16.

Early senescence-induced immunosuppressive β-cell secretome prevents type 1 diabetes

(Submitter supplied) During the progression of type 1 diabetes (T1D), β-cells are exposed to significant stress and therefore require adaptive responses to survive. The adaptive mechanisms that can preserve β-cell function and survival in the face of autoimmunity remain unclear. Here we show that deletion of the unfolded protein response genes, Atf6α or Ire1α, in β-cells of NOD mice prior to insulitis generates a p21-driven early senescence phenotype and altered β-cell secretome that significantly enhances leukemia inhibitory factor-mediated recruitment of M2 macrophages to the islets. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
7 Samples
Download data: XLSX
Series
Accession:
GSE239947
ID:
200239947
17.

RNA sequencing of control and PTPN2 knocked down transcriptomes in EndoC- H1 cells with or without the treatment of pro-inflammatory cytokines

(Submitter supplied) Type 1 diabetes (T1D) results from autoimmune destruction of β-cells in the pancreas. Protein tyrosine phosphatases (PTPs) are candidate genes for T1D and play a key role in autoimmune disease development and β-cell function. Here, we assessed the global protein and individual PTP profile in the pancreas from diabetic NOD mice treated with anti-CD3 monoclonal antibody and IL-1 receptor antagonist (IL-1RA). more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
18 Samples
Download data: XLS, XLSX
Series
Accession:
GSE172148
ID:
200172148
18.

Alpha, beta and delta cells reponse to IFNγ

(Submitter supplied) Characterization of mouse pancreatic alpha, beta and delta cells responses to IFNγ
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
18 Samples
Download data: RESULTS
Series
Accession:
GSE221081
ID:
200221081
19.

Gene expression of PD-L1 high and low pancreatic beta cells, after 20h of incubation wiht 50pg.mL of IFNγ.

(Submitter supplied) Characterization of FACS-sorted PD-L1 high and low mouse pancreatic beta cells after 20h of incubation with low dose of IFNγ.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
11 Samples
Download data: RESULTS
Series
Accession:
GSE221078
ID:
200221078
20.

Loss of tetraspanin-7 expression reduces pancreatic beta-cell exocytosis Ca2+ sensitivity but has limited effect on systemic metabolism

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL24247 GPL21697
10 Samples
Download data
Series
Accession:
GSE213731
ID:
200213731
Format
Items per page
Sort by

Send to:

Choose Destination

Supplemental Content

db=gds|term=|query=1|qty=3|blobid=MCID_666bd6296e9d376f232356e1|ismultiple=true|min_list=5|max_list=20|def_tree=20|def_list=|def_view=|url=/Taxonomy/backend/subset.cgi?|trace_url=/stat?
   Taxonomic Groups  [List]
Tree placeholder
    Top Organisms  [Tree]

Find related data

Recent activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...
Support Center