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The effect of extreme hyperglycemia on the expression program of the human beta cell line EndoC-betaH2

ABSTRACT: The effect of extreme hyperglycemia on the expression program of the human beta cell line EndoC-betaH2

PROVIDER: PRJNA877196 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21437905.fastq.gz	Fastqsanger.gz
	SRR21437906.fastq.gz	Fastqsanger.gz
	SRR21437907.fastq.gz	Fastqsanger.gz
	SRR21437908.fastq.gz	Fastqsanger.gz
	SRR21437909.fastq.gz	Fastqsanger.gz

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The effect of extreme hyperglycemia on the expression program of the human beta cell line EndoC-betaH2

Project description:Our in vivo Insulin-rtTA;TET-DTA mouse model of severe hyperglycemia revealed that proloned exposure to very high glucose levels inhibits cell cycle entry and progression of pancreatic beta cells. To investigate the molecular mechanisms responsible for this observation and the relevance to human beta cells, we performed an in vitro experiment on EndoC-betaH2 mimiking the in vivo conditions and subjected them to RNAseq analysis.

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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.

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