41c3b744-1081-49a1-bfc5-662031585fe6 - samples
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00001005523 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:RNAsequencing data from human pancreatic islets from 191 donors, Lund University. Processed for the Inspire consortium.
| EGAD00001005512 | EGA
Project description:Genotyping data (Imputed) from human pancreatic islets from 191 donors from Lund that were analysed as part of the Inspire consortium.
| EGAD00001005521 | EGA
Project description:Expression profiling of cell cycle genes in human pancreatic islets with and without type 2 diabetes Islets from cadaver donors were provided by the Nordic Islet Transplantation Programme (www.nordicislets.org), Uppsala University. The microarrays were performed using GeneChipM-BM-. Human Gene 1.0 ST whole transcript according to Affymetrix standard protocol.
2013-03-15 | E-GEOD-44035 | biostudies-arrayexpress
Project description:Here we harnessed the potential of expression arrays in 89 human pancreatic islet donors (different levels of blood glucose (HbA1c)) to identify genes regulated in this relevant tissue for type 2 diabetes (T2D). Islets from cadaver donors were provided by the Nordic Islet Transplantation Programme (www.nordicislets.org), Uppsala University. The microarrays were performed using GeneChipM-BM-. Human Gene 1.0 ST whole transcript according to Affymetrix standard protocol.
2014-07-17 | E-GEOD-50397 | biostudies-arrayexpress
Project description:Pancreatic islet beta cell failure causes type 2 diabetes (T2D). The IMIDIA consortium has used a strategy entailing a stringent comparative transcriptomics analysis of islets isolated enzymatically or by laser microdissection from two large cohorts of non-diabetic (ND) and T2D organ donors (OD) or partially pancreatectomized patients (PPP). This work led to the identification of a signature of genes that were differentially expressed between T2D and ND regardless of the sample type (OD or PPP). This signature includes 19 genes, of which 9 have never been previously reported to be differentially expressed in T2D islets. The PPP cohort also includes samples from individuals with impaired glucose tolerance (IGT) or recent onset diabetes associated with a pancreatic exocrine disorder (T3cD). Notably, none of the 19 signature genes of T2D islets were significantly dysregulated in islets of subjects with IGT or T3cD, suggesting that their changed expression reflects beta cell deterioration rather than a deficit preceding it.
2017-12-09 | GSE76895 | GEO
Project description:Pancreatic islet beta cell failure causes type 2 diabetes (T2D). The IMIDIA consortium has used a strategy entailing a stringent comparative transcriptomics analysis of islets isolated enzymatically or by laser microdissection from two large cohorts of non-diabetic (ND) and T2D organ donors (OD) or partially pancreatectomized patients (PPP). This work led to the identification of a signature of genes that were differentially expressed between T2D and ND regardless of the sample type (OD or PPP). This signature includes 19 genes, of which 9 have never been previously reported to be differentially expressed in T2D islets. The PPP cohort also includes samples from individuals with impaired glucose tolerance (IGT) or recent onset diabetes associated with a pancreatic exocrine disorder (T3cD). Notably, none of the 19 signature genes of T2D islets were significantly dysregulated in islets of subjects with IGT or T3cD, suggesting that their changed expression reflects beta cell deterioration rather than a deficit preceding it.
2017-12-09 | GSE76894 | GEO
Project description:Pancreatic islets are central in type 2-diabetes development, which coincides with increased activity of innate immunity. Intriguingly, human pancreatic islets express many complement genes. The most highly expressed gene was the complement inhibitor CD59 that is GPI anchored to the cell membrane, which unexpectedly was found in high amounts intracellularly in beta cells. Silencing of CD59 strongly suppressed insulin secretion. Importantly, this suppression was unrelated to established CD59 functions, but rather depletion of intracellular CD59. Imaging experiments identified a distal site of inhibition in the exocytotic pathway, but prior to emptying of the insulin granules. Proximity Ligation Assays pin-pointed the mechanism to impaired turnover of exocytosis-regulating SNARE-proteins and CD59 was detected in complex with VAMP2 and syntaxin. CD59 was downregulated by 24-h glucose incubations in human islets, rat cell lines and in islets from three rodent diabetes models. Islets from cadaver donors were provided by the Nordic Islet Transplantation Programme (www.nordicislets.org), Uppsala University. The microarrays were performed using GeneChipM-BM-. Human Gene 1.0 ST whole transcript according to Affymetrix standard protocol.
2014-03-02 | E-GEOD-54279 | biostudies-arrayexpress
Project description:Type 1 diabetes (T1D) is caused by the autoimmune destruction of insulin-producing pancreatic beta cells, leading to life-long dependence on exogenous insulin. Profiling immune cells that infiltrate islets would be invaluable to understanding how beta cell destruction occurs. However, human pancreatic samples demonstrating active infiltration and beta cell destruction are rare. Alternatively, peri-pancreatic lymph nodes (pLNs) or other secondary lymphoid organs may harbor immune cells which participate in memory responses that drive T1D autoimmunity. To study the immune response throughout T1D onset and disease, lymphocytes from pLNs, mesenteric lymph nodes (mesLNs), and the spleen were collected from human T1D, auto-antibody positive (AAb+), and normal donors (NDs) enrolled in the Human Pancreas Analysis Program (HPAP). Tissue immune cell identity, phenotype, and transcriptional status was analyzed using Cellular Indexing of Transcriptomes and Epitopes by Sequencing (CITEseq). Lymphocytes from 20 pLN, 12 mesLN, and 18 spleen samples spanning 6 ND, 7 AAb+, and 7 T1D donors were thawed and processed through the CITEseq pipeline. At least 5 donors per disease group had a paired pLN and spleen sample, with at least 3 of the 5 donors per disease group having a paired mesLN sample, allowing for cross-tissue immune status comparison spanning multiple stages of disease onset. The dataset provides one of the first and largest CITEseq datasets on human AAb+ and T1D samples publicly available.
2023-01-03 | GSE221787 | GEO
Project description:Type 1 diabetes is an autoimmune disease caused by the destruction of the insulin producing beta cells. We characterized the gene expression profile of pancreatic tissue from four type 1 diabetes patients (Cases 1-4), who died at different stages of the disease (onset and longstanding) by microarray analysis. All samples from patients and controls were obtained after death, at the time of organ donation. Pancreatic blocks from the four diabetic patients and three organ donors (Controls 1-3) were obtained and snap frozen. At the same time, islets from Cases 1 and 4 were isolated from a piece of the pancreas tail by enzymatic digestion (using automated method and handpicking) and snap frozen. Islets from three different organ donors (Controls 4-6) were obtained similarly to those of the diabetic patients. Both pancreatic blocks and islets were stored in liquid nitrogen until the mRNA extraction. For pancreas gene expression profiles, we compared data from three blocks of each of the four type 1 diabetic pancreas with pancreases data from the Controls 1-3. For islets expression profile, we compared data from Cases 1 and 4 islets with islets data from the Controls 4-6. <br><br>
2009-12-01 | E-MEXP-1140 | biostudies-arrayexpress
Project description:7 RNA-Seq datasets in human pancreatic islets from 7 donors, where islets were using low (4mM) glucose conditions.
| EGAD00001005208 | EGA