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Genomic data archive from the Network for Pancreatic Organ donors with Diabetes

ABSTRACT: Genomic data archive from the Network for Pancreatic Organ donors with Diabetes

PROVIDER: PRJNA821969 | ENA |

REPOSITORIES: ENA

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Genomic data archive from the Network for Pancreatic Organ donors with Diabetes

Project description:Genomic data archive from the Network for Pancreatic Organ donors with Diabetes

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A genomic data archive from the Network for Pancreatic Organ donors with Diabetes.

Project description:The Network for Pancreatic Organ donors with Diabetes (nPOD) is the largest biorepository of human pancreata and associated immune organs from donors with type 1 diabetes (T1D), maturity-onset diabetes of the young (MODY), cystic fibrosis-related diabetes (CFRD), type 2 diabetes (T2D), gestational diabetes, islet autoantibody positivity (AAb+), and without diabetes. nPOD recovers, processes, analyzes, and distributes high-quality biospecimens, collected using optimized standard operating procedures, and associated de-identified data/metadata to researchers around the world. Herein describes the release of high-parameter genotyping data from this collection. 372 donors were genotyped using a custom precision medicine single nucleotide polymorphism (SNP) microarray. Data were technically validated using published algorithms to evaluate donor relatedness, ancestry, imputed HLA, and T1D genetic risk score. Additionally, 207 donors were assessed for rare known and novel coding region variants via whole exome sequencing (WES). These data are publicly-available to enable genotype-specific sample requests and the study of novel genotype:phenotype associations, aiding in the mission of nPOD to enhance understanding of diabetes pathogenesis to promote the development of novel therapies.

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Project description:Islet function diminishes with age and as such the incidence of type 2 diabetes increases. The cause of this is unknown. In this study whole islets were extracted with laser capture microdissection from organ donors 1-81 years of age. Increasing age was associated with a downregulation of pathways associated with the cell cycle and increase in markers of senescence e.g. CDKN2A. Among novel genes increasing with age was SPP1.

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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.

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Single cell RNA-seq of human pancreatic endocrine cells from Juvenile, adult control and type 2 diabetic donors.

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