LncRNA SCIRT in hypoxia/reoxygenation.
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ABSTRACT:
PROVIDER: PRJNA794182 | ENA |
REPOSITORIES: ENA
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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: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: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: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
Project description:Intermittent hypoxia is a common stressor in estuarine and coastal habitats due to the diurnal and tidal cycles of oxygen availability. Oxygen deficiency results in energy stress by limiting aerobic ATP production, while reoxygenation may lead to oxidative injury due to the excessive production of reactive oxygen species (ROS) in mitochondria. Mitochondria are a key intracellular target of hypoxia-reoxygenation (H/R) stress due to their central role in ATP production, ROS generation and stress signaling. Marine intertidal bivalves such as the Pacific oyster Crassostrea gigas are adapted to frequent H/R cycles in the intertidal zone and maintain mitochondrial integrity and aerobic function despite frequent oxygen fluctuations. To gain insight into the molecular responses of mitochondria of the hypoxia-tolerant Pacific oyster to H/R stress, we studied changes in oxidative phosphorylation (OXPHOS) capacity, proton leak and activity of the electron transport system enzymes (ETS) in gill mitochondria of C. gigas. We furthermore investigated shifts in mitochondrial proteome and phosphoproteome after 24 h of hypoxia and 1 h of post-hypoxic recovery. Oyster mitochondria maintained normal ETS and OXPHOS capacity during H/R stress, despite a slight but significant decline in cytochrome c oxidase (Complex IV) activity after reoxygenation. Fifty total proteins and 36 phosphoproteins were differentially abundant in mitochondria of H/R exposed oysters compared with the controls. Rearrangements of the mitochondrial (phospho)proteome during H/R stress involved upregulation of mitochondrial ETS (most notably Complexes I and IV) and iron-binding proteins (frataxin and ferrochelatase) as well as suppression of the metabolic pathways that channel electrons to ubiquinone, possibly as a mechanism to limit ROS production due to the iron overload and reverse flow of electrons through ETS. H/R stress also led to upregulation of a mitophagic activator serine/threonine protein phosphatase PGAM5 and dephosphorylation of metalloendopeptidase OMA1 indicating stimulation of mitochondrial quality control mechanisms during reoxygenation. Changes in the overall abundance and phosphorylation levels of several key proteins involved in the mitochondrial protein homeostasis (including subunits of the mitochondrial ribosome, mitochondrial inner membrane translocase and elongation factor G) are consistent with the suppression of the protein synthesis during hypoxia, likely as an energy-saving mechanism. Overall, our study indicates that shifts in the mitochondrial (phospho-)proteome play an important role in responses of oysters to H/R stress and might complement adaptations of anaerobic metabolism and metabolic rate depression in ensuring hypoxic survival and rapid recovery in this hypoxia-tolerant intertidal species.
2021-11-04 | PXD011365 | Pride
Project description:To investigate the transcriptional response of tumor adaptation to reoxygenation, breast cancer cells MCF-7 was cultured under 0.5% of hypoxia for 24h followed by 24h of reoxygenation in normoxia. Cells were harvested respectively at 0, 1, 4, 8, 12, and 24h during reoxygenation. Total RNA obtained from human breast cancer cell line MCF-7 were collected respectively at 0, 1, 4, 8, 12 and 24 hours after reoxygenation.
2012-01-01 | E-GEOD-30019 | biostudies-arrayexpress
Project description:Ischemia-reperfusion injury to the central nervous system (CNS) often causes severe complications. Hypoxia/reoxygenation (H/R) is one of the most common and detrimental internal environmental changes experienced by local cells and is often used to simulate the process of ischemia-reperfusion in vitro. The activation of endogenous neural stem cells (NSCs) is considered a promising therapeutic strategy for nerve repair after injury. However, the specific biological processes and molecular mechanisms of NSC activation remain unclear.
2023-03-31 | GSE221842 | GEO
Project description:Oxygen (O2) is a double-edged sword to cells for while it is vital for energy production in all aerobic animals and insufficient O2 (hypoxia) can lead to cell death, the reoxygenation of hypoxic tissues may trigger the generation of reactive oxygen species (ROS) that can destroy any biological molecule. Indeed, both hypoxia and hypoxia-reoxygenation (H/R) stress are harmful, and may play a critical role in the pathophysiology of many human diseases such as myocardial ischemia and stroke. Therefore, understanding how animals adapt to hypoxia and H/R stress is critical for developing better treatments for these diseases. Previous studies showed that the neuroglobin GLB-5(Haw) is essential for the fast recovery of the nematode Caenorhabditis elegans (C. elegans) from H/R stress. Here, we characterize the changes in neuronal gene expression during the adaptation of worms to hypoxia and recovery from H/R stress. Our analysis show that innate immunity genes are differentially expressed during both adaptation to hypoxia and recovery from H/R stress.
2017-05-09 | GSE93149 | GEO