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CD81 marks immature and dedifferentiated pancreatic β-cells

ABSTRACT: CD81 marks immature and dedifferentiated pancreatic β-cells

PROVIDER: PRJNA680167 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13106844.fastq.gz	Fastqsanger.gz
	SRR13106845.fastq.gz	Fastqsanger.gz
	SRR13106846.fastq.gz	Fastqsanger.gz
	SRR13106847.fastq.gz	Fastqsanger.gz
	SRR13106848.fastq.gz	Fastqsanger.gz

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CD81 marks immature and dedifferentiated pancreatic β-cells.

Project description:ObjectiveIslets of Langerhans contain heterogeneous populations of insulin-producing β-cells. Surface markers and respective antibodies for isolation, tracking, and analysis are urgently needed to study β-cell heterogeneity and explore the mechanisms to harness the regenerative potential of immature β-cells.MethodsWe performed single-cell mRNA profiling of early postnatal mouse islets and re-analyzed several single-cell mRNA sequencing datasets from mouse and human pancreas and islets. We used mouse primary islets, iPSC-derived endocrine cells, Min6 insulinoma, and human EndoC-βH1 β-cell lines and performed FAC sorting, Western blotting, and imaging to support and complement the findings from the data analyses.ResultsWe found that all endocrine cell types expressed the cluster of differentiation 81 (CD81) during pancreas development, but the expression levels of this protein were gradually reduced in β-cells during postnatal maturation. Single-cell gene expression profiling and high-resolution imaging revealed an immature signature of β-cells expressing high levels of CD81 (CD81high) compared to a more mature population expressing no or low levels of this protein (CD81low/-). Analysis of β-cells from different diabetic mouse models and in vitro β-cell stress assays indicated an upregulation of CD81 expression levels in stressed and dedifferentiated β-cells. Similarly, CD81 was upregulated and marked stressed human β-cells in vitro.ConclusionsWe identified CD81 as a novel surface marker that labels immature, stressed, and dedifferentiated β-cells in the adult mouse and human islets. This novel surface marker will allow us to better study β-cell heterogeneity in healthy subjects and diabetes progression.

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CD81 marks immature and dedifferentiated pancreatic β-cells

Project description:We performed 3 single-cell RNAseq experiments to dissect the postnatal islet heterogeneity. In order to reach our goal, we used the Fltp lineage tracing (FltpiCre mTmG) mouse line. Thus we used mice at the age of 16 days, isolated islets of Langerhans from them and sorted via flow cytometry the three Fltp subpopulations.

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RNA-seq of purified human pancreatic dedifferentiated acinar cells and duct cells

Project description:Pancreatic acinar cells can dedifferentiate upon tissue injury and acquire ductal characteristics. This acquisition of duct cell features is critical in tumor development. Nevertheless, duct cells themselves are less prone for development of PDAC (pancreatic ductal adenocarcinoma) than dedifferentiated acini. We aimed to clarify which genes are unique for dedifferentiated acini. Mixed exocrine preparations of acinar and duct cells were obtained from human pancreatic donor organs and cultured to induce dedifferentiation. We lineage-labeled and FACS-purified these human dedifferentiated acinar cells and compared them to duct cells from the same donor (n=5).

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Transcription profiling by array of a directed differentiation time course converting human embryonic stem cells (hES) into immature pancreatic beta cell precursors

Project description:Transcriptional profiling of a directed differentiation time course converting human embryonic stem cells (hES) into immature pancreatic beta cell precursors.

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microRNA profiling by array of a directed differentiation time course converting human embryonic stem cells (hES) into immature pancreatic beta cell precursors

Project description:miRNA transcript profiling of a directed differentiation time course converting human embryonic stem cells (hES) into immature pancreatic beta cell precursors.

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Project description:Expansion of beta cells from the limited number of adult human islet donors is an attractive prospect for increasing cell availability for cell therapy of diabetes. However, while evidence supports the replicative capacity of adult beta cells in vivo, attempts at expanding human islet cells in tissue culture resulted in loss of beta-cell phenotype. Using a genetic lineage-tracing approach we have provided evidence for massive proliferation of beta-cell-derived (BCD) cells within these cultures. Expansion involves dedifferentiation resembling epithelial-mesenchymal transition (EMT). Epigenetic analyses indicate that key beta-cell genes maintain a partially open chromatin structure in expanded BCD cells, although they are not transcribed. Here we report that BCD cells can be induced to redifferentiate by a combination of soluble factors. The redifferentiated cells express beta-cell genes, store insulin in typical secretory vesicles, and release it in response to glucose. The redifferentiation process involves mesenchymal-epithelial transition, as judged from changes in gene expression. Moreover, inhibition of the EMT effector SLUG using shRNA results in stimulation of redifferentiation. BCD cells also give rise at a low rate to cells expressing other islet hormones, suggesting transition through an islet progenitor-like stage during redifferentiation. These findings suggest that ex-vivo expansion of adult human islet cells is a promising approach for generation of insulin-producing cells for transplantation, as well as basic research, toxicology studies, and drug screening. Gene expression was studied in unexpanded islets (4 donors), expanded and dedifferentiated islet cells (4 donors), and re-differentiated islet cells (3 donors). The experiment was performed in 3 batches (see Date in the description table below).

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Progenitor Cell Marker Aldehyde Dehydrogenase 1a3 Defines a Subset of Failing Pancreatic Beta Cells in Diabetic Mice

Project description:Insulin-producing beta cells become dedifferentiated during diabetes progression. An impaired ability to select substrates for oxidative phosphorylation, or metabolic inflexibility, sets the stage for progression from beta cell dysfunction to beta cell dedifferentiation. In this study, we sought to isolate and functionally characterize failing beta cells, as a preliminary step to identify pathways to reverse dedifferentiation. Using various experimental models of diabetes, we found a striking enrichment in the expression of aldehyde dehydrogenase 1 isoform A3 (ALDH+) as beta cells become dedifferentiated. Flow-sorted ALDH+ islet cells demonstrate impaired glucose-induced insulin secretion, are depleted of Foxo1 and MafA, and include a Neurogenin3-positive subset. RNA sequencing analysis demonstrates that ALDH+ cells are characterized by: (i) impaired oxidative phosphorylation and mitochondrial complex I, IV, and V; (ii) activated RICTOR; and (iii) progenitor cell markers. We propose that impaired mitochondrial function marks the progression from metabolic inflexibility to dedifferentiation in the natural history of beta cell failure. RNA-Sequencing analysis of 2 different cell types in 2 different genotype categories.

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