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ABSTRACT: mRNA sequencing (RNA-sequencing ) of human β-cell model EndoC-βH1

PROVIDER: PRJNA563975 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10069968_1.fastq.gz	Fastqsanger.gz
	SRR10069968_2.fastq.gz	Fastqsanger.gz
	SRR10069969_1.fastq.gz	Fastqsanger.gz
	SRR10069969_2.fastq.gz	Fastqsanger.gz
	SRR10069970_1.fastq.gz	Fastqsanger.gz

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EndoC-βH1 multiomic profiling defines gene regulatory programs intrinsic to human β cell identity and function

Project description:EndoC-βH1 is emerging as a critical human β cell model to study the genetic and environmental etiologies of β cell (dys)function and diabetes. Comprehensive knowledge of its molecular landscape is lacking, yet required, for effective use of this model. Here, we report chromosomal (spectral karyotyping), genetic (genotyping), epigenomic (ChIP-seq and ATAC-seq), chromatin interaction (Hi-C and Pol2 ChIA-PET), and transcriptomic (RNA-seq and miRNA-seq) maps of EndoC-βH1. Analyses of these maps define known (e.g., PDX1 and ISL1) and putative (e.g., PCSK1 and mir-375) β cell-specific transcriptional cis-regulatory networks and identify allelic effects on cis-regulatory element use. Importantly, comparison with maps generated in primary human islets and/or β cells indicates preservation of chromatin looping but also highlights chromosomal aberrations and fetal genomic signatures in EndoC-βH1. Together, these maps, and a web application we created for their exploration, provide important tools for the design of experiments to probe and manipulate the genetic programs governing β cell identity and (dys)function in diabetes.

2019-01-08 | GSE118588 | GEO

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.

Project description: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. Resulting cells were distributed as ready to use EndoC-βH5 cells. We performed comparative transcriptome analysis with EndoC-βH1 cells , extensive functional and immunological assays. RNA-seq confirmed abundant expression of beta cell transcription factors and functional markers, including incretin receptors.

2023-07-20 | GSE224660 | GEO

Enhanced crosslinking and immunoprecipitation analysis of human fetal β-cells

Project description:N6-methyladenosine (m6A) is the most abundant chemical modification in mRNA, and plays important roles in human embryonic stem cell pluripotency, maintenance, and differentiation. However, the role of m6A and the precise mechanisms involved during the development of β-cells are unexplored. Here, we performed enhanced crosslinking and immunoprecipitation (eCLIP) assays to identify m6A sites regulated by METTL14 in EndoC-βh1 human fetal β-cells.

2024-06-13 | GSE236324 | GEO

Dexamethasone effect on gene expression in human pancreatic islets and human pancreatic EndoC-βH1 cells

Project description:To investigate the glucocorticoid-mediated transcriptomic changes in human pancreatic islets and the human insulin-secreting EndoC-βH1 cells in order to uncover genes and molecular pathways involved in β-cell steroid stress-response processes.

2023-03-16 | GSE225901 | GEO

RNAsequencing of control and STAT3 knocked down transriptomes of EndoC cells

Project description:Most obese and insulin resistant individuals do not develop diabetes. This is the result of the capacity of β-cells to adapt and produce enough insulin to cover the needs of the organism. The underlying mechanism of β-cell adaptation in obesity, however, remains unclear. Previous studies have suggested a role for STAT3 in mediating β-cell development and human glucose homeostasis, but little is known about its role in β-cells in obesity. We observed enhanced cytoplasmatic expression of STAT3 in severe obese and diabetic subjects. To address the functional role of STAT3 in adult β-cells, we generated mice with tamoxifen-inducible partial or full deletion of STAT3 in β-cells and fed them a high fat diet before analysis. Interestingly, β-cell homozygous and heterozygous STAT3 deficient obese mice showed glucose intolerance when compared to controls. Gene expression analysis by RNA-seq showed reduced expression of mitochondrial genes in STAT3 knocked-down human EndoC-βH1 cells and was confirmed in FACS-purified β-cells from STAT3 deficient mice. Moreover, knockdown of STAT3 impaired mitochondria activity in EndoC-βH1 and human islets, suggesting a mechanism for STAT3-regulated β-cell function. We propose non-canonical STAT3 activity as a marker of β-cell identity, improving glucose induced insulin secretion in obesity.

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

Project description: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.

2023-04-01 | GSE218735 | GEO

Effect of TUNAR silencing and GSK3 inhibition on human b-cell transcriptome

Project description:The aim of the study is to identify the target genes of long noncoding RNA TUNAR in human EndoC-βH1 cells with or without treatment of GSK3 inhibitor.

2017-06-01 | GSE99503 | GEO

Transcription and splicing regulation by NLRC5 shape the interferon response in human pancreatic β-cells [iPSC scRNAseq]

Project description:IFNa is a key regulator of the dialogue between pancreatic β-cells and the immune system in early type 1 diabetes (T1D). IFNa up-regulates HLA class I expression in human β-cells fostering autoantigen presentation to the immune system. We observed by bulk and single cell RNA sequencing that exposure of human induced pluripotent-derived islet-like cells to IFNa induces expression of HLA class I and of other genes involved in antigen presentation, including the transcriptional activator NLRC5. We next evaluated the global role of NLRC5 in human insulin-producing EndoC-βH1 and human islets cells by RNA sequencing and targeted gene/protein determination. NLRC5 regulates expression of HLA class I expression and related genes and of chemokines. NLRC5 also mediates the effects of IFNa on alternative splicing, a generator of β-cell neoantigens, suggesting that it is a central mediator of the effects of IFNa on β-cells that contribute to trigger and amplify autoimmunity in T1D.

2022-09-14 | GSE203384 | GEO

Transcription and splicing regulation by NLRC5 shape the interferon response in human pancreatic β-cells [RNA-seq]

2022-09-14 | GSE202852 | GEO

Characterization of human β-cell lines

Project description:Electrophysiological properties of human β-cell lines EndoC-βH1 and βH2 conform with human β-cells

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