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Effects of DNA topoisomerase inhibitor acriflavine on endothelial gene expression and chromatin accessibility (RNA-Seq)

ABSTRACT: Effects of DNA topoisomerase inhibitor acriflavine on endothelial gene expression and chromatin accessibility (RNA-Seq)

PROVIDER: PRJNA736696 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14779081.fastq.gz	Fastqsanger.gz
	SRR14779082.fastq.gz	Fastqsanger.gz
	SRR14779083.fastq.gz	Fastqsanger.gz
	SRR14779084.fastq.gz	Fastqsanger.gz
	SRR14779085.fastq.gz	Fastqsanger.gz

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Effects of DNA topoisomerase inhibitor acriflavine on endothelial gene expression and chromatin accessibility

Project description:Effects of DNA topoisomerase inhibitor acriflavine on endothelial gene expression and chromatin accessibility

| PRJNA736692 | ENA

Effects of DNA topoisomerase inhibitor acriflavine on endothelial gene expression and chromatin accessibility (ATAC-Seq)

Project description:Effects of DNA topoisomerase inhibitor acriflavine on endothelial gene expression and chromatin accessibility (ATAC-Seq)

| PRJNA736697 | ENA

Effects of DNA topoisomerase inhibitor acriflavine on endothelial gene expression under hypoxic conditions

Project description:RNA-Seq of human endothelial cells treated with acriflavine (ACF) with or without hypoxia revealed massive changes on gene expression. These were non-randomly and potentially due to DNA topoisomerase inhibition rather than HIF inhibition. Surprisingly, in contrast to protein-coding genes, RNA-Seq yielded that an exceeding number of lncRNAs is upregulated.

2022-01-19 | GSE186297 | GEO

Effects of DNA topoisomerase inhibitor acriflavine on endothelial gene expression under hypoxic conditions

Project description:Effects of DNA topoisomerase inhibitor acriflavine on endothelial gene expression under hypoxic conditions

| PRJNA773246 | ENA

Effects of DNA topoisomerase inhibitor acriflavine on endothelial gene expression and chromatin accessibility (RNA-Seq)

Project description:RNA-Seq of human endothelial cells treated with ACF revealed massive changes on gene expression. These were non-randomly and strongly conserved to murine lung endothelial cells potentially due to DNA topoisomerase inhibition rather than HIF inhibition. Surprisingly, in contrast to protein-coding genes, RNA-Seq yielded that an exceeding number of lncRNAs is upregulated, e.g. FENDRR, H19, HIF1α-AS1 and FLJ31356, whereas BOLA3-AS1 and MEG3 were strongly downregulated. ATAC-Seq demonstrated that ACF leads to strong changes on chromatin accessibility on lncRNA promoters.

2022-01-19 | GSE176555 | GEO

Effects of DNA topoisomerase inhibitor acriflavine on endothelial gene expression and chromatin accessibility (ATAC-Seq)

2022-01-19 | GSE176554 | GEO

Effects of DNA topoisomerase inhibitor acriflavine on endothelial gene expression and chromatin accessibility

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-01-19 | GSE176556 | GEO

DNA topoisomerase inhibition with the HIF inhibitor acriflavine promotes transcription of lncRNAs in endothelial cells.

Project description:The transcription factor hypoxia-inducible factor 1 (HIF1) is an important driver of cancer and is therefore an attractive drug target. Acriflavine (ACF) has been suggested to inhibit HIF1, but its mechanism of action is unknown. Here we investigated the interaction of ACF with DNA and long non-coding RNAs (lncRNAs) and its function in human endothelial cells. ACF promoted apoptosis and reduced proliferation, network formation, and angiogenic capacity. It also induced changes in gene expression, as determined by RNA sequencing (RNA-seq), which could not be attributed to specific inhibition of HIF1. A similar response was observed in murine lung endothelial cells. Although ACF increased and decreased a similar number of protein-coding genes, lncRNAs were preferentially upregulated under normoxic and hypoxic conditions. An assay for transposase accessibility with subsequent DNA sequencing (ATAC-seq) demonstrated that ACF induced strong changes in chromatin accessibility at lncRNA promoters. Immunofluorescence showed displacement of DNA:RNA hybrids. Such effects might be due to ACF-mediated topoisomerase inhibition, which was indeed the case, as reflected by DNA unwinding assays. Comparison with other acridine derivatives and topoisomerase inhibitors suggested that the specific function of ACF is an effect of acridinium-class compounds. This study demonstrates that ACF inhibits topoisomerases rather than HIF specifically and that it elicits a unique expression response of lncRNAs.

| S-EPMC8844413 | biostudies-literature

Trichophyton rubrum transcriptome in response to acriflavine

Project description:Purpose: The dermatophyte Trichophyton rubrum is an anthropophilic filamentous fungus that infects keratinized tissues and is the most common etiologic agent isolated in cases of human dermatophytoses. To better understand the molecular effects of stress responses and fungal adaptability, we evaluated the effects of acriflavine, a cytoxic drug, on T. rubrum transcriptome in a time-course assay using high-throughput RNA-seq technology. Results: RNA-seq generated approximately 200 million short reads that were mapped to the Broad Institute’s Dermatophyte Comparative Database before differential gene expression analysis. A subset of 490 genes modulated in response to stress caused T. rubrum exposure to acriflavine were identified. These genes are involved in various cellular processes such as oxidation-reduction reactions, transmembrane transport, metal ion binding, and pathogenicity. The genes involved in pathogenicity were down-regulated, suggesting that this drug interferes with virulence factors that allow the establishment and maintenance of host infection. Conclusion: The results obtained in this large-scale analysis provide insights into the molecular events underlying the stress responses of T. rubrum Acriflavine.

2015-03-05 | GSE40425 | GEO

Endothelial inflammation inhibitor screen

Project description:[placeholder] Endothelial inflammation is an important factor in endothelial dysfunction. TNFa and IFNg induce unique inflammation state in ECs, which is synergistically amplified when both are combined. Here we propose targeted inhibition of endothelial inflammation employing an unbiased proteomics drug inhibitor screen of NFKB and JAK/STAT targets. We show STAT6 regulates the expression of a wide range of angiogenic proteins. Inhibition of with JAK1 inhibitor itacitinib nullifies the IFNg inflammation response without off target proteomic effects. IKK2/STAT3 combined inhibition inhibited both inflammation states. Interestingly, the majority of TNFa+IFNg induced proteins could be inhibited by either JAK1 or IKK2/STAT3 inhibition, reiterating the synergetic nature of this inflammation state. Finally, we show the relation of VWF with inflammation. In conclusion we employ proteomic drug screen to assess potential drug candidates to inhibit endothelial inflammation, which highlights the feasibility of targeting the endothelium and provides an interesting outlook for future studies.

2025-07-17 | PXD058294 | Pride

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