Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The hypoxia induced changes in mRNA in RNA-induced silencing complexes in hypoxia exposed human endothelial cells

ABSTRACT: The hypoxia induced changes in mRNA in RNA-induced silencing complexes in hypoxia exposed human endothelial cells

PROVIDER: PRJNA786499 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR17139536.fastq.gz	Fastqsanger.gz
	SRR17139537.fastq.gz	Fastqsanger.gz
	SRR17139538.fastq.gz	Fastqsanger.gz
	SRR17139539.fastq.gz	Fastqsanger.gz
	SRR17139540.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 14

Similar Datasets

The hypoxia induced changes in mRNA in RNA-induced silencing complexes in hypoxia exposed human endothelial cells

Project description:What governs the transition between the two HIFs (the HIF switch) and the role of miRNAs in this regulation is not completely clear. Using genome-wide expression studies on the miRNA content of RNA-induced silencing complex (RISC) in HUVECs exposed to hypoxia compared to the global miRNA-Seq analysis revealed dramatic differences between the two. In our analyses, compared the miRNA and mRNA levels in RISC at 2 hours (mainly HIF-1 driven), 8 hours (HIF-1 and HIF-2 elevated), and 16 hours (mainly HIF-2 driven) in a gene ontology context. This allowed for determining the direct impact of the miRNAs in modulating the cellular signaling pathways involved in the adaptive response. Furthermore, we demonstrate that the hypoxic levels of the vast majority of HIF-1-dependent miRNAs (including miR-210-3p) are also HIF-2 dependent, and that HIF-2 specifically governs the expression of 11 specific miRNAs

2022-09-15 | GSE190240 | GEO

The hypoxia induced changes in miRNA in RNA-induced silencing complexes and HIFs induced miRNAs in human endothelial cells

Project description:The hypoxia induced changes in miRNA in RNA-induced silencing complexes and HIFs induced miRNAs in human endothelial cells

| PRJNA786527 | ENA

The hypoxia induced changes in miRNA in RNA-induced silencing complexes and HIFs induced miRNAs in human endothelial cells

2022-09-15 | GSE190242 | GEO

Hypoxia Induced Pulmonary Hypertension

Project description:Here we investigated the protein composition of the main pulmonary artery (MPA), distal pulmonary arteries (DPA) distal whole lung (DWL) of early stage hypoxia (using a neonatal bovine calf model) and late stage hypoxia (using adult steers with hypoxia-induced PH) using high resolution mass spectrometry. Compartment-resolved analysis allowed for quantitative measurements of proteins from cellular, soluble ECM and insoluble ECM fractions

2022-10-06 | MSV000090482 | MassIVE

siRNA-mediated silencing of ORAI3 in MDA-MB-468 breast cancer cells exposed to hypoxia

Project description:Analysis of the effect of siRNA-mediated silencing of ORAI3 in MDA-MB-468 basal-like breast cancer cells exposed to 48 and 72 h hypoxia

2019-02-11 | GSE107692 | GEO

Transcription profiling of Arabidopsis roots and shoots in response to hypoxia using immunopurified mRNA-ribosome complexes - SuperSeries

Project description:This SuperSeries is composed of the following subset Series:; GSE14493: Immunopurified mRNA-ribosome complexes expose cell-type specific plasticity during hypoxia in Arabidopsis root tips; GSE14502: Immunopurified mRNA-ribosome complexes expose cell-type specific plasticity in response to hypoxia in Arabidopsis Experiment Overall Design: Refer to individual Series

2009-10-20 | E-GEOD-14578 | biostudies-arrayexpress

Impact of Nfat5 on normoxia- and hypoxia-exposed mouse lung endothelial cells

Project description:Chronic hypoxia causes detrimental structural alterations in the lung, which are partially dependent on stress responses of the endothelium. In this context, we revealed that hypoxia-exposed murine lung endothelial cells (MLEC) activate nuclear factor of activated T-cells 5 (NFAT5/TonEBP) - a transcription factor that adjusts the cellular transcriptome to cope with multiple environmental stressors. Here, we studied the impact of NFAT5 on hypoxia-induced gene expression in MLEC by comparing the transcriptome of control and Nfat5-deficient MLEC, which were isolated from mouse lungs after exposure to normoxia and hypoxia for 7 days and processed for scRNA seq.

2024-08-08 | GSE255681 | GEO

The hypoxia-induced changes in miRNA-mRNA in RNA-induced silencing complexes and HIF-2 induced miRNAs in human endothelial cells.

Project description:The cellular adaptive response to hypoxia relies on the expression of hypoxia-inducible factors (HIFs), HIF-1 and HIF-2. HIFs regulate global gene expression changes during hypoxia that are necessary for restoring oxygen homeostasis and promoting cell survival. In the early stages of hypoxia, HIF-1 is elevated, whereas at the later stages, HIF-2 becomes the predominant form. What governs the transition between the two HIFs (the HIF switch) and the role of miRNAs in this regulation are not completely clear. Genome-wide expression studies on the miRNA content of RNA-induced silencing complexes (RISC) in HUVECs exposed to hypoxia compared to the global miRNA-Seq analysis revealed very specific differences between these two populations. We analyzed the miRNA and mRNA composition of RISC at 2 h (mainly HIF-1 driven), 8 h (HIF-1 and HIF-2 elevated), and 16 h (mainly HIF-2 driven) in a gene ontology context. This allowed for determining the direct impact of the miRNAs in modulating the cellular signaling pathways involved in the hypoxic adaptive response. Our results indicate that the miRNA-mRNA RISC components control the adaptive responses, and this does not always rely on the miRNA transcriptional elevations during hypoxia. Furthermore, we demonstrate that the hypoxic levels of the vast majority of HIF-1-dependent miRNAs (including miR-210-3p) are also HIF-2 dependent and that HIF-2 governs the expression of 11 specific miRNAs. In summary, the switch from HIF-1 to HIF-2 during hypoxia provides an important level of miRNA-driven control in the adaptive pathways in endothelial cells.

| S-EPMC9220987 | biostudies-literature

Endothelial senescence mediates hypoxia-induced vascular remodeling by modulating PDGFB expression

Project description:Uncontrolled accumulation of pulmonary artery smooth muscle cells (PASMC) to the distal pulmonary arterioles (PAs) is one of the major characteristics of pulmonary hypertension (PH). Cellular senescence contributes to aging and lung diseases associated with PH and links to PH progression. However, the mechanism by which cellular senescence controls vascular remodeling in PH is not fully understood. The levels of senescence marker, p16INK4A and senescence-associated β-galactosidase (SA-β-gal) activity are higher in PA endothelial cells (ECs) isolated from idiopathic pulmonary arterial hypertension (IPAH) patients compared to those from healthy individuals. Hypoxia-induced accumulation of α-smooth muscle actin (αSMA)-positive cells to the PAs is attenuated in p16fl/fl-Cdh5(PAC)-CreERT2 (p16iΔEC) mice after tamoxifen induction. We have reported that endothelial TWIST1 mediates hypoxia-induced vascular remodeling by increasing platelet-derived growth factor (PDGFB) expression. Transcriptomic analyses of IPAH patient or hypoxia-induced mouse lung ECs reveal the alteration of senescence-related gene expression and their interaction with TWIST1. Knockdown of p16INK4A attenuates the expression of PDGFB and TWIST1 in IPAH patient PAECs or hypoxia-treated mouse lungs and suppresses accumulation of αSMA–positive cells to the supplemented ECs in the gel implanted on the mouse lungs. Hypoxia-treated mouse lung EC-derived exosomes stimulate DNA synthesis and migration of PASMCs in vitro and in the gel implanted on the mouse lungs, while p16iΔEC mouse lung EC-derived exosomes inhibit the effects. These results suggest that endothelial senescence controls αSMA–positive cell proliferation and migration in PH through TWIST1-PDGFB signaling.

2022-10-15 | PXD033549 | Pride

Interplay between Two Paralogous Human Silencing Hub (HuSH) Complexes in Regulating LINE-1 Element Silencing

Project description:Interplay between Two Paralogous Human Silencing Hub (HuSH) Complexes in Regulating LINE-1 Element Silencing

| PRJNA980677 | ENA