Comparative Transcriptomic Analysis of Vascular Endothelial Cells after Hypoxia/Reoxygenation Induction
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA604628 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Hypoxia and re-oxygenation are common features in many physiological and pathological processes such as, inflammation and tumorigenesis. Vascular endothelial (VEC) participates in the regulation of a variety of important balances in the body and the regulation of cellular functions, plays an important role in the reaction of organs such as ischemia, hypoxia, and inflammatory immunity.
2020-03-20 | GSE144715 | GEO
Project description:lncRNA SCIRT in hypoxia/reoxygenation.
| PRJNA794182 | ENA
Project description:Purpose: Study hypoxia and reoxygenation induced changes in genome-wide gene expression Methods: Using the MCF7 breast epithelial adenocarcinoma cell line as a model, we studied epigenomic reprogramming as a function of fluctuating oxygen tension. To this end, we performed a transcriptomics analysis in MCF7 cells subjected to changes in oxygenation (i.e. acute hypoxia, chronic hypoxia, reoxygenation). Results: Global downregulation upon hypoxia; partial restore on reoxygenation. Conclusions: Our data show that oxygen availability dynamically regulates gene transcription.
2016-11-01 | GSE70805 | GEO
Project description:To know effects of long noncoding RNA (lncRNA) SCIRT in hypoxia/reoxygenation (H/R). We compared expression profiles of human umbilical vein endothelial cells (HUVECs) under normal condition, H/R condition without SCIRT knockdown, and H/R condition with SCIRT knockdown.
2022-06-15 | GSE193048 | GEO
Project description:Gene expression analysis of 7d-old Arabidopsis seedlings exposed to short term (2 h) hypoxia, long term (9 h) hypoxia, and 1 h reoxygenation after long term (9 h) hypoxia to evaluate the regulation of gene expression at the level of translation. Keywords: Time Course, hypoxia recovery, polysomal mRNA, IP RNA, polysomes, hypoxia stress, reoxygenation, translational control.
2008-07-22 | GSE9719 | GEO
Project description:Gene expression analysis of 7d-old Arabidopsis seedlings exposed to short term (2 h) hypoxia, long term (9 h) hypoxia, and 1 h reoxygenation after long term (9 h) hypoxia to evaluate the regulation of gene expression at the level of translation. Experiment Overall Design: 30 samples, 5 conditions (2 hr hypoxia stress, 2hr non-stress, 9 hr hypoxia stress , 9 hr non-stress, 9 hr hypoxia with 1 hr recovery), 2 RNA pools (Total mRNA and polysomal mRNA), 3 replicates
2008-10-20 | E-GEOD-9719 | biostudies-arrayexpress
Project description:Purpose: Study hypoxia and reoxygenation induced changes in genome-wide H3K4me3 and H3K27me3 occupancy Methods: Using the MCF7 breast epithelial adenocarcinoma cell line as a model, we studied epigenomic reprogramming as a function of fluctuating oxygen tension. To this end, we combined chromatin-immunoprecipitation and deep-sequencing analysis to identify H3K4me3-marks and H3K27me3-marks in MCF7 cells subjected to changes in oxygenation (i.e. acute hypoxia, chronic hypoxia, reoxygenation). Results: H3K4me3 and H3K27me3-marks showed a rapid global increase at specific sites throughout the genome under hypoxia, both genic and inter-genic, that was partly restored upon reoxygenation. Conclusions: Our data show that oxygen availability dynamically regulates the epigenetic state of the genome.
2016-11-01 | GSE71030 | GEO
Project description:High-altitude pulmonary hypertension (HAPH) is a severe and progressive disease caused by chronic hypoxia and subsequent pulmonary vascular remodeling. No cure is currently available owing to an incomplete understanding about vascular remodeling. It is believed that hypoxia-induced diseases can be prevented by treating hypoxia. Thus, this study aimed to determine whether daily short-duration reoxygenation at sea level attenuates pulmonary hypertension under high-altitude hypoxia. To this end, a simulated 5,000-m hypoxia rat model was used to evaluate the effect of short-duration reoxygenation. Results show that intermittent, not continuous, short-duration reoxygenation effectively attenuates hypoxia-induced pulmonary hypertension. The mechanisms underlining the protective effects involved that intermittent, short-duration reoxygenation prevented functional and structural remodeling of pulmonary arteries and proliferation, migration, and phenotypic conversion of pulmonary artery smooth muscle cells under hypoxia. The specific genes or potential molecular pathways responsible for mediating the protective effects were also characterised by RNA sequencing.This study is novel in revealing a new potential method in preventing high-altitude pulmonary hypertension. It gives insights into the selection and optimisation of oxygen supply schemes in high-altitude areas.
2020-11-06 | GSE160926 | GEO
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
Project description:Hypoxia is a characteristic feature of marine environments and a major stressor for marine organisms inhabiting benthic and intertidal zones. Several studies have explored the responses of these organisms to hypoxic stress at the whole organism level with a focus on energy metabolism and mitochondrial response, but the instrinsic mitochondrial responses that support the organelle’s function under hypoxia and reoxygenation (H/R) stress are not well understood. We studied the effects of acute H/R stress (10 min anoxia followed by 15 min reoxygenation) on mitochondrial respiration, production of reactive oxygen species (ROS) and posttranslational modifications (PTM) of the proteome in a marine facultative anaerobe, the blue mussel Mytilus edulis. The mussels’ mitochondria showed increased OXPHOS respiration and suppressed proton leak resulting in a higher coupling efficiency after H/R stress. ROS production decreased in both the resting (LEAK) and phosphorylating (OXPHOS) state indicating that M. edulis is able to prevent oxidative stress and mitochondrial damage during reoxygenation. Hypoxia did not stimulate the rearrangement of the mitochondrial supercomplexes but impacted the mitochondrial phosphoproteome including the proteins involved in OXPHOS, amino acid and fatty acid catabolism, and protein quality control. This study indicates that mussels’ mitochondria possess intrinsic mechanisms (including regulation via PTM mechanisms such as reversible protein phosphorylation) that ensure high respiratory flux and mitigate oxidative damage during H/R stress and contribute to the hypoxia-tolerant mitochondrial phenotype of this metabolically plastic species.
2021-11-25 | PXD027955 | Pride