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Transcriptomic and epigenetic analysis of iPSC-endothelial cells treated with statin

ABSTRACT: Transcriptomic and epigenetic analysis of iPSC-endothelial cells treated with statin

PROVIDER: PRJNA663305 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12637011_1.fastq.gz	Fastqsanger.gz
	SRR12637011_2.fastq.gz	Fastqsanger.gz
	SRR12637012_1.fastq.gz	Fastqsanger.gz
	SRR12637012_2.fastq.gz	Fastqsanger.gz
	SRR12637013_1.fastq.gz	Fastqsanger.gz

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Transcriptomic and epigenetic analysis of iPSC-endothelial cells treated with statin

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Project description:Statins prevent cardiovascular disease via their salutary function as inhibitors of cholesterol biosynthesis and mediators of pleiotropic effects on the cardiovascular system. The current study focuses on the class effect of statins on the transcriptome of human iPSC-derived cardiomyocytes (iPSC-CMs), applied at serum peak concentrations. We report a comprehensive transcriptomic analysis of iPSC-CMs derived from four healthy donors and different differentiation batches following treatment with fluvastatin, simvastatin, atorvastatin, and lovastatin. Our data display dynamic transcriptional networks and reveal a statin-induced molecular signature in iPSC-CMs independent of genetic background and technical variability. Finally, in-depth pathway enrichment analysis uncovers that all statins affect mainly metabolic properties of iPSC-CMs and particularly the regulation of cholesterol biosynthesis and fatty acid metabolism. Our study provides a global insight into the cardiomyocyte effects of statins revealing novel aspects of their role on cardiomyocyte metabolic regulation, when applied at clinically relevant concentrations.

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Expression data of statin treated HUVEC cells transfected siRNA KLF2 or KLF4.

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Expression data of statin treated HUVEC cells transfected siRNA KLF2 or KLF4.

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Primary human hepatocyte transcriptomic statin response

Project description:We have previously identified a number of statin-responsive genes in human cell lines, but in some cases, these findings may not be relevant in vivo. Here, we statin exposed primary human hepatocytes from four different donors to identify statin-responsive genes in this biologically relevant cell type. We also compared the effects of statin on gene expression between these primary cells and our previous datasets in other cell lines to identify overlapping effects of interest.

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Liver transcriptome of statin-treated patients

Project description:Background: Clinical data identified an association between the use of HMG-CoA reductase inhibitors (statins) and incident diabetes in patients with underlying diabetes risk factors such as obesity, hypertension and dyslipidemia. The molecular mechanisms however are unknown. Methods: An observational cross-sectional study included 910 severely obese patients, mean (SD) body mass index 46.7 (8.7), treated with or without statins (ABOS cohort: a biological atlas of severe obesity). Data and sample collection took place in France between 2006 and 2016. Transcriptomic signatures of statin treatment in human liver obtained from genome-wide transcriptomic profiling of five different statin drugs using microarrays were correlated to clinico-biological phenotypes and also assigned to biological pathways and mechanisms. Results: We determined the hepatic, statin-related gene signature from genome-wide transcriptomic profiling in severely obese patients with varying degrees of glucose tolerance and cardio-metabolic comorbidities. Patients on statin treatment showed higher diabetes prevalence (OR=2.67; 95%CI, 1.60-4.45; P= 0.0002) and impairment of glucose homeostasis. This phenotype was associated with molecular signatures of increased hepatic de novo lipogenesis (DNL) via activation of sterol regulatory element-binding protein-1 (SREBP1) and concomitant upregulation of the expression of key genes in both fatty acid and triglyceride metabolism. Conclusions: DNL gene activation profile in response to statins was associated with insulin resistance and the diabetic status of the patients. Identified molecular signatures thus suggest that statin treatment increases the risk for diabetes in humans at least in part via induction of DNL.

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