Project description:The physiological behavior of mouse embryonic stem cells (mESCs) is intricately regulated by microenvironmental oxygen levels, with normoxia (21% O₂) and hypoxia (1-5% O₂) exhibiting distinct impacts on self-renewal, differentiation, and metabolic adaptation. However, the epigenetic mechanisms underlying oxygen-dependent gene expression remain poorly characterized. This study investigates the dynamic alterations of histone modifications associated with transcriptional regulation—specifically, the active promoter mark H3K4me3 (trimethylation of histone H3 lysine 4) and the enhancer mark H3K27ac (acetylation of histone H3 lysine 27)—in mESCs under normoxic versus hypoxic conditions. Utilizing chromatin immunoprecipitation followed by sequencing (ChIP-seq), we systematically mapped genome-wide occupancy patterns of H3K4me3 and H3K27ac, identifying oxygen-sensitive epigenetic landscapes that correlate with differential gene activity. Comparative analysis revealed hypoxia-induced redistribution of these marks at loci linked to pluripotency maintenance, hypoxia-responsive pathways (e.g., HIF-1α targets), and metabolic reprogramming. These findings highlight the role of oxygen tension in reshaping the epigenetic architecture of mESCs, providing insights into how microenvironmental cues fine-tune stem cell functionality through histone modification dynamics. This work advances our understanding of epigenetic plasticity in stem cells and may inform strategies for optimizing in vitro culture conditions or manipulating cell fate under physiological or pathological oxygen gradients.
Project description:Extracellular vesicles (EVs) represent a diverse group of small membrane-encapsulated particles and provide a universal molecular cell-cell communication system. Hypoxia is a typical condition in solid tumors, and cancer-derived EVs support growth and invasion of tissues by tumor cells. EVs were purified from cell culture medium by ultracentrifugation followed by size exclusion chromatography with Exo-spin™ columns (Cell Guidance Systems Ltd). We performed proteomic analysis of five hypoxia/normoxia pairs of EV samples; each of these replicates for either hypoxia or normoxia was analyzed in duplicates. Obtained data were compared with proteomics analysis of corresponding cell culture media supernatants (SN) after EV removal with 100 000 g ultracentrifugation. We found that exposure of tumor cells to hypoxia (1% oxygen) induced EV secretion, altered EV sizes, and led to notable changes in the EV protein cargo in comparison to normoxia.
Project description:To better understand the effect of hypoxia, RNA-Seq technology was used to profile the Aspergillus fumigatus during adaptation to hypoxia at 12, 24 and 36 h time points. Four samples examined: from the fungus grown under normoxia and hypoxia conditions
Project description:Lymphatic endothelial cells were grown under normoxia, hypoxia (1% 0xygen) and conditioned medio from NSLCN growth under normoxia or hypoxia. Gene expression was measured and comparition between samples performed Experiment Overall Design: RNA from different donnors where extracted, pooled to avoid interindividual differences and labelled. Microarrays hybridized and analyzed
Project description:Purpose: The goal of this study is to investigate the role of interplay between circadian clock and oxygen-sensing pathways in determining myogenic progenitor cell fate. Methods: Total RNAs were extracted from wild-type and Bmal1-/- myoblasts following exposure to normoxia (21% O2) or hypoxia (1% O2) for 6 hours, and subjected to RNA-sequencing. Results: There were significantly up-regulated (443 in normoxia versus 477 in hypoxia) and down-regulated (745 in normoxia versus 796 in hypoxia) genes in Bmal1-/- cells compared to wild-type, with a large degree of overlap between hypoxia and normoxia, although the fold change of differential gene expression was generally greater under hypoxia versus normoxia. Conclusion: Loss of Bmal1 in myoblasts leads to a premature differentiation-prone transcriptome, which was exaggerated following exposure to hypoxia.
Project description:Lysates of Mycobacterium tuberculosis (H37Rv auxotroph mc(2)6020) grown under various conditions (normoxia, hypoxia, reactivation from hypoxia) probed the serine hydrolase probe with ActivX-desthiobiotin FP.
Project description:Here we compare the transcriptional profiles of SW480 cells with ITPR3 or RELB knockout with control cells under normoxia and hypoxia.
Project description:Estrogen receptor alpha plays a critical role in breast cancer and is a major target in endocrine therapy. HIF-1 alpha have been associated with ER alpha and predict a worse outcome. Recent studies indicate that histone demethylase JMJD2B is a HIF-1 alpha target. However, little is known about the biological functions of JMJD2B, especially in breast cancer. To elucidate the mechanism by which JMJD2B reguates gene expression in normoxia and hypoxia, MCF-7 breast cancer cells were depleted forJMJD2B in normoxia and hypoxia. Our results provide insight into JMJD2B regulation of gene expression in breast cancer cells in normoxia and hypoxia.
Project description:Hypoxia leads to the aggregation of PD-L1 on the cell membrane without altering the overall protein expression level of PD-L1. Identify differentially expressed genes in the hypoxic transcriptome to reveal the key proteins involved in PD-L1 membrane trafficking, using samples of SCC25 cells treated with normoxia and hypoxia for 12 hours.