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Effect of NFE2L2 silencing on miRNA profile of human aortic endothelial cells (HAECs) in response to GDF-15 and SDF-1

ABSTRACT: Effect of NFE2L2 silencing on miRNA profile of human aortic endothelial cells (HAECs) in response to GDF-15 and SDF-1

PROVIDER: PRJNA430405 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6498860.fastq.gz	Fastqsanger.gz
	SRR6498870.fastq.gz	Fastqsanger.gz
	SRR6498861.fastq.gz	Fastqsanger.gz
	SRR6498871.fastq.gz	Fastqsanger.gz
	SRR6498862.fastq.gz	Fastqsanger.gz

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Effect of NFE2L2 silencing on miRNA profile of human aortic endothelial cells (HAECs) in response to GDF-15 and SDF-1

Project description:Nrf2 is a transcription factor playing an essential role in stress response. A knowledge of the significance of Nrf2 in cell function has not, as yet, reached out beyond transactivation of gene expression. This paper shows that GDF-15 and SDF-1-induced angiogenesis strongly depends on Nrf2 presence, but is not related to its transcriptional activity. We propose, that Nrf2 serves as a protein restraining Keap1, its known transcriptional repressor. Deficiency of Nrf2 protein available for Keap1 leads to overabundance of RhoGAP1, the protein regulating Cdc42 activity, and impairs podosome assembly, thereby indisposing actin rearrangements, and preventing angiogenesis. These activities can be rescued by concomitant deletion of RhoGAP1 or Keap1. We suggest that a new Nrf2 function of a Keap1 scavenger implies revising the established murine model of Nrf2 deficiency as a transcriptional knock out (tKO) mouse. The N-terminal fragment of Nrf2, containing Neh2 domain binding Keap1, is present in these animals. Thus, regarding the function of Nrf2 as a protein sequestering Keap1, both published and unpublished data on Nrf2-Keap1 duet may gain new interpretation.

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Transcriptional profiling of trimethylamine N-oxide (TMAO) stimulated human aortic endothelial cells (HAECs)

Project description:Purpose: The goals of this study were to identify preferential gene expression signatures that are unique to HAECs stimulated with the uremic toxin, TMAO, to accelerate vascular inflammation associated with chronic kidney diseases. Methods and results: HAECs were treated with TMAO (600 µM) for 18 hours, and RNAs were collected to generate mRNA transcription profiles. Transcriptional profiling revealed a unique TMAO stimulated HAECs relative to a non-stimulated control HAECs. Conclusion: Our study represents the first detailed analysis of TMAO treated HAECs transcriptome.

2023-01-03 | GSE216833 | GEO

ChIP-seq of H3K27acethylation of human aortic endothelial cells (HAECs) treated with Cobalt chloride (CoCl2)

Project description:Endothelial-to-mesenchymal transition (EndMT) is a fundamental process in vascular remodeling, and hypoxia is known to induce EndMT and involved in cardiovascular disease development. Cobalt chloride (CoCl2), a chemical inducer of hypoxia-inducible factor-1 (HIF-1) could influence cellular function and its differentiation. However, exact molecular mechanism how stabilization of HIF-1 by cobalt chloride in human primary ECs affects cellular behavior and EndMT process is largely unknown. In this study, we performed ChIP-seq for H3K27ac in human aortic endothelial cells (HAECs) treated with CoCl2

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Transcriptome analysis of human aortic endothelial cells (HAECs) with KLF11 knockdown

Project description:Transcriptome analysis of human aortic endothelial cells (HAECs) with KLF11 knockdown

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Transcriptome analysis of human aortic endothelial cells (HAECs) with KLF11 knockdown

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Transcriptional profiling of trimethylamine N-oxide (TMAO) stimulated human aortic endothelial cells (HAECs)

Project description:Transcriptional profiling of trimethylamine N-oxide (TMAO) stimulated human aortic endothelial cells (HAECs)

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