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Dual-RNA-seq of Acinetobacter baumannii ABC141 inside endothelial cells EA.hy926

ABSTRACT: Dual-RNA-seq of Acinetobacter baumannii ABC141 inside endothelial cells EA.hy926

PROVIDER: PRJNA1272120 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR33831800.fastq.gz	Fastqsanger.gz
	SRR33831801.fastq.gz	Fastqsanger.gz
	SRR33831802.fastq.gz	Fastqsanger.gz
	SRR33831803.fastq.gz	Fastqsanger.gz
	SRR33831804.fastq.gz	Fastqsanger.gz

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Dual-RNA-seq of Acinetobacter baumannii ABC141 inside endothelial cells EA.hy926

Project description:Acinetobacter baumannii poses a substantial global health threat, causing severe multi-drug-resistant infections in hospitalized patients. Circulating clinical isolates present remarkable diversity, with a proportion capable of establishing a transient intracellular niche suitable for persistence, multiplication, and spread. Yet, it remains unknown which bacterial factors mediate the formation and maintenance of this niche, especially within non-phagocytic cells, nor what host responses are elicited. This work demonstrates that the invasive A. baumannii ABC141 strain does not secrete ammonia in endothelial cells as previously shown for other A. baumannii strains multiplying within macrophages but resides in an acidic vacuole devoid of active lysosomal degradative enzymes. Using a Dual-RNAseq approach, we mapped the host and bacterial gene expression during the replicative stage of the infection. An atypical hypoxia cell response was observed without significant induction of the HIF1 pathway, with no metabolic shift or disturbance of mitochondria. Surprisingly, ABC141 efficiently grew in hypoxic conditions in culture and within host cells. In addition, we found a bacterial signature reflective of an adaptation to a nutrient-deprived environment. Our work also highlights a differential role for ABC141 secretion systems, with the T1SS assisting intracellular multiplication and the T2SS required for host cell invasion, implicating for the first time the T2SS in the intracellular lifecycle of invasive ABC141 in endothelial cells.

2025-06-04 | GSE299021 | GEO

Endothelial dysfunction in NR2F2-silenced cells - EA.hy926 cells model

Project description:Endothelial dysfunction in NR2F2-silenced cells - EA.hy926 cells model

| PRJNA779018 | ENA

Transcriptomic analysis of human vascular endothelial cell line (EA.hy926) exposed to okadaic acid

Project description:As the climate changes due to global warming, the frequency of appearance of marine-derived toxins increases. In particular, the need to investigate marine-derived toxins for which toxicity has not yet been identified is emerging. Blood vessels are passageways through which compounds entering the body move to various organs and are the sites first exposed to compounds. Therefore, it is important to know the effects of compounds on blood vessels when they enter the body. In this study, the human vascular endothelial cell line EA.hy926 was exposed to the marine toxins OA (IC20; 42.9 nM) and the mechanism of toxicity was investigated at the transcriptome level. Quantseq 3' mRNA sequencing was performed by extracting RNA from EA.hy926 cells exposed to the toxins. Differentially expressed genes were determined based on fold change ≥ 1.5 and P value < 0.05.

2024-05-18 | GSE267374 | GEO

Inside Plectosphaerellaceae

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The expression profile in EA.hy926 cells after exposure to hypoxic conditions was evaluated by RNA-sequencing.

Project description:Hypoxia is an imbalance between oxygen supply and demand that occurs in embryonic development, as well as in pathological situations such as cancer, ischemic heart disease, and wound healing. To cope with decreased oxygen concentrations, a series of biological processes that endothelial cells participate in such as angiogenesis, are transcriptionally activated. In this work, we performed RNA-sequencing to profile activated genes in EA.hy926 cells after 8 hours of hypoxia, to reveal the changes of gene expression profile in endothelial cells under hypoxia.

2021-06-09 | GSE176365 | GEO

Transcriptomic analysis of human vascular endothelial cell line (EA.hy926) exposed to okadaic acid

Project description:Transcriptomic analysis of human vascular endothelial cell line (EA.hy926) exposed to okadaic acid

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Characterization of two distinct immortalized endothelial cell lines HMEC-1 and EA.hy926 for in vitro studies: exploring the impact of calcium electroporation, Ca2+ signaling and transcriptome profile

Project description:The vascular endothelium consists of endothelial cells (ECs) with important biological functions and their impairment is associated with various pathologies. ECs vary based on tissue origin and gene expression, while their functionality depends on calcium (Ca2+) signaling. In tumors, disruption of Ca2+ homeostasis after calcium electroporation (CaEP) has been shown to elicit an enhanced antitumor effect with only minimal effect on normal tissue. The difference in response to CaEP was not only observed between cancer and normal cells, but also between different endothelial cell lines. Although several vascular EC models have been developed, there is a lack of understanding regarding the molecular basis that could help explain different responses of normal tissue to CaEP. Therefore, our study aims to determine the effect of CaEP on established immortalized human EC lines EA.hy926 and HMEC-1 in terms of cytoskeleton, Ca2+ kinetics and differences in gene expression involved in regulation of Ca2+ signaling and homeostasis.

2024-02-21 | GSE244042 | GEO

Characterization of A. baumannii Mitomycin C (MMC) response

Project description:Transcriptional profiling of A. baumannii ATCC 17978 comparing treated-MMC cultures with non-MMC treated cultures Two-condition experiment A. baumannii 17978 MMC+ vs A. baumannii 17978 MMC-. Biological replicates:3, Technical replicates:2

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Characterizing Acinetobacter baumannii desiccation tolerance.

Project description:Desiccation tolerance has been implicated as an important characteristic that potentiates the spread of the bacterial pathogen Acinetobacter baumannii through hospitals on dry surfaces. Despite the potential importance of this stress response, scarce information is available describing the underlying mechanisms of A. baumannii desiccation tolerance. Here we characterize the factors influencing desiccation survival of A. baumannii. At the macroscale level, we find that desiccation tolerance is influenced by cell density, growth phase, and desiccation medium. Our transcriptome analysis indicates that desiccation represents a unique state for A. baumannii compared to commonly studied growth conditions and strongly influences pathways responsible for proteostasis. Remarkably, we find that an increase in total cellular protein aggregates, which is often considered deleterious, correlates positively with the ability of A. baumannii to survive desiccation. We show that artificially inducing protein aggregate formation increases desiccation survival, and more importantly, that proteins incorporated into cellular aggregates can retain activity. Our results suggest that protein aggregates may promote desiccation tolerance in A. baumannii through preserving and protecting proteins from damage during desiccation until rehydration occurs.

2018-10-27 | GSE111383 | GEO

Endothelial dysfunction in NR2F2-silenced cells - EA.hy926 cells model

Project description:Orphan nuclear receptor chicken ovalbumin upstream promoter transcription factor 2 (COUPTF2; NR2F2) is highly expressed in endothelial cells (ECs) and Nr2f2 knockout produces lethal cardiovascular defects. In humans, NR2F2 mutations result in both congenital heart disease and diaphragmatic hernia, conditions associated with the development of pulmonary arterial hypertension (PAH). However, COUPTF2 functions in mature endothelium are uncertain. NR2F2 knockdown in primary human endothelial cells (ECs) led to an interferon-biased inflammatory response, endothelial-to-mesenchymal transition, proliferation, hypermigration, apoptosis-resistance and mitochondrial dysfunction. These phenotypic changes were associated with AKT activation and increased Dickkopf-1 (DKK1) expression, a Wnt/β-catenin pathway inhibitor. DKK1 was also elevated in patients with PAH and secreted in response to loss of bone morphogenetic receptor type 2 (BMPR2), the archetypal PAH-associated genetic defect. Together, these findings demonstrate that endothelial NR2F2 suppresses inflammation and proliferation. Thus, NR2F2 loss disrupts EC homeostasis and may promote pathologic vascular remodeling in the development of PAH.

2023-05-31 | GSE188465 | GEO

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