Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA297774 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2558120.fastq.gz | Fastqsanger.gz | |||
| SRR2558130.fastq.gz | Fastqsanger.gz | |||
| SRR2558140.fastq.gz | Fastqsanger.gz | |||
| SRR2558150.fastq.gz | Fastqsanger.gz | |||
| SRR2558160.fastq.gz | Fastqsanger.gz |
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Project description:To understand organ (dys)function it is important to have a complete inventory of its cell types and the corresponding markers that unambiguously identify these cell types. This is a challenging task, in particular in human tissues, because unique cell-type markers are typically unavailable, necessitating the analysis of complex cell type mixtures. Transcriptome-wide studies on pancreatic tissue are typically done on pooled islet material. To overcome this challenge we sequenced the transcriptome of thousands of single pancreatic cells from deceased organ donors with and without type 2 diabetes (T2D) allowing in silico purification of the different cell types. We identified the major pancreatic cell types resulting in the identification of many new cell-type specific and T2D-specific markers. Additionally we observed several subpopulations within the canonical pancreatic cell types, which we validated in situ. This resource will be useful for developing a deeper understanding of pancreatic biology and diabetes mellitus. Human cadaveric pancreata were used to extract islets of Langerhans, which were kept in culture until single-cell dispersion and FACS sorting. Single-cell transcriptomics was performed on live cells from this mixture using CEL-seq or on cells stained for CD63, CD13, TGFBR3 or CD24 and CD44. The RaceID algorithm was used to identify clusters of cells corresponding to the major pancreatic cell types and to mine for novel cell type-specific genes as well as subpopulations within the known pancreatic cell types.
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Project description:Mechanisms driving sex differences across islet cells is unknown. Thus, studying sex differences in islet regulation and function represent a unique avenue to understand the sex-specific heterogeneity in β cell failure in diabetes. We examined sex and race differences in human pancreatic islets from 15 donors using an orthogonal series of experiments including single cell RNA-seq (scRNA-seq), single nucleus assay for transposase-accessible chromatin sequencing (snATAC-seq), dynamic hormone secretion, and bioenergetics.
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Project description:Blood glucose levels are tightly controlled by the coordinated action of at least five cell types constituting pancreatic islets. Changes in the proportion and/or function of these cells are associated with genetic and molecular pathophysiology of monogenic, type 1, and type 2 diabetes (T2D). Cellular heterogeneity impedes precise understanding of the molecular components of each islet cell type that govern islet dysfunction, particularly the less abundant delta and gamma/pancreatic polypeptide (PP) cells. Here, we report single cell transcriptomes for 617 islet cells after profiling ~1000 cells from non-diabetic (ND) and T2D human organ donors. Analyses of non-diabetic single cell transcriptomes identified distinct alpha, beta, delta, and PP/gamma cell-type signatures. Genes linked to rare and common forms of islet dysfunction and diabetes were expressed in the delta and PP/gamma cell types. Moreover, this study revealed that delta cells specifically express receptors that receive and coordinate systemic cues from the leptin, ghrelin, and dopamine signaling pathways implicating them as integrators of central and peripheral metabolic signals into the pancreatic islet. Finally, single cell transcriptome profiling revealed genes differentially regulated between T2D and ND alpha, beta, and delta cells that were undetectable in paired whole islet analyses. This study thus identifies fundamental cell type-specific features of pancreatic islet (dys)function and provides a critical resource for comprehensive understanding of islet biology and diabetes pathogenesis. Grant ID: Award No. W81XWH-16-1-0130 Grant title: Peer Reviewed Medical Research Program Funding Source: Assistant Secretary of Defense for Health Affairs Affiliation: Jackson Laboratory for Genomic Medicine, Farmington, CT Name: Michael Stitzel
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Project description:Blood glucose levels are tightly controlled by the coordinated action of at least five cell types constituting pancreatic islets. Changes in the proportion and/or function of these cells are associated with genetic and molecular pathophysiology of monogenic, type 1, and type 2 diabetes (T2D). Cellular heterogeneity impedes precise understanding of the molecular components of each islet cell type that govern islet dysfunction, particularly the less abundant delta and gamma/pancreatic polypeptide (PP) cells. Here, we report single cell transcriptomes for 617 islet cells after profiling ~1000 cells from non-diabetic (ND) and T2D human organ donors. Analyses of non-diabetic single cell transcriptomes identified distinct alpha, beta, delta, and PP/gamma cell-type signatures. Genes linked to rare and common forms of islet dysfunction and diabetes were expressed in the delta and PP/gamma cell types. Moreover, this study revealed that delta cells specifically express receptors that receive and coordinate systemic cues from the leptin, ghrelin, and dopamine signaling pathways implicating them as integrators of central and peripheral metabolic signals into the pancreatic islet. Finally, single cell transcriptome profiling revealed genes differentially regulated between T2D and ND alpha, beta, and delta cells that were undetectable in paired whole islet analyses. This study thus identifies fundamental cell type-specific features of pancreatic islet (dys)function and provides a critical resource for comprehensive understanding of islet biology and diabetes pathogenesis. Grant ID: Award No. W81XWH-16-1-0130 Grant title: Peer Reviewed Medical Research Program Funding Source: Assistant Secretary of Defense for Health Affairs Affiliation: Jackson Laboratory for Genomic Medicine, Farmington, CT Name: Michael Stitzel
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