Human macrophages exposed to hypoxia
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE4630 | GEO | 2006/04/11
SECONDARY ACCESSION(S): PRJNA95529
REPOSITORIES: GEO
Similar Datasets
Project description:The aim of this study was to investigate the effects of hypoxia on human macrophages Experiment Overall Design: Cultured macrophages from 4 donors were exposed to normoxia (21% oxygen) or hypoxia (0% oxygen) for 24 h. Two μg RNA from 4 donors incubated at normoxia and 4 donors at hypoxia was pooled respectively and these 2 pools were used for the target preparation and analyzed on duplicate DNA microarrays. Comparisons were made between the expression profile from macrophages exposed to hypoxia and the expression profile from the control normoxic macrophages to identify genes regulated during hypoxia.
2008-06-13 | E-GEOD-4630 | biostudies-arrayexpress
Project description:Ischemia exists in many diseased tissues including arthritic joints, atherosclerotic plaques and malignant tumors. Macrophages accumulate in these sites and upregulate genes in response to the hypoxia present. We used Illumina beadarrays to investigate the effect of hypoxia (18h at 0.1% oxygen) on gene expression by human monocyte-derived macrophages in vitro.
2009-05-14 | GSE16099 | GEO
Project description:ChIP-seq targeting H3K9ac and H3K27me3 histone modifications was carried out on macrophages isolated from aortas of mice exposed to intermittent hypoxia or room air conditions.
2017-06-12 | GSE86851 | GEO
Project description:Employing single-cell transcriptomic analyses, we investigated the repertoire and functional profiles of pulmonary interstitial macrophages in response to exposure at 0, 1, 3, 7, and 21 days of hypobaric hypoxia (at an altitude of 5,486 meters). The repertoire and functional profiles of interstitial macrophages (IMs) undergo dynamic changes based on the duration of hypoxia exposure. Acute hypoxia leads to type 1 acute inflammatory responses in most IM populations, which largely subside by Day 7. The resolution of the inflammatory phase is succeeded by the accumulation of dysregulated IMs, contributing to abnormal pulmonary vascular repair and remodeling. The classical and alternative complement pathways may play distinct roles in regulating early inflammation and later vascular remodeling phases in pulmonary hypertension (PH) pathogenesis. These findings highlight the dynamic nature of IMs, emphasizing that understanding the timing and mechanisms through which they influence PH pathogenesis will contribute to the development of IM-specific therapeutic targets.
2024-04-15 | GSE254606 | GEO
Project description:Diabetic foot ulcers (DFUs) are characterized by a chronic inflammation state which prevents cutaneous wound healing, andDFUs eventually lead to infection and leg amputation. Macrophages located in DFUs are locked in an pro-inflammatory phenotype. In this study, the effect of hyperglycemia and hypoxia on the macrophage phenotype was analyzed. For this purpose, a microarray was performed to study the gene expression profile of macrophages cultivated in a high glucose concentration. Hyperglycemia upregulated the expression of pro-inflammatory cytokines such as TNF-α, IL-1, IL-6, chemokines and downregulatd the expression of two receptors involved in phagocytosis (CD 36 and Class B scavenger type I receptors). In addition, eleven anti-apoptotic factors were upregulated whereas three pro-apoptotic ones were downregulated. Subsequently, the contribution of hypoxia and hyperglycemia to chronic inflammation and their potential synergic effect was evaluated on activated THP-1 derived macrophages. A long term post activation effect (17 hours) was only observed on the upregulation of pro-inflammatory cytokines when hypoxia was combined with a high glucose concentration. In contrast, hyperglycemia and hypoxia did not have any effect on wound healing molecules such as TGF-β1. Taken together, the results show that hyperglycemia acts in synergy with hypoxia to maintain a chronic inflammation state in macrophages.
2019-07-24 | GSE132187 | GEO
Project description:Our previous studies demonstrated that exposing cells to acute hypoxic conditions in vitro (24 h at 1% oxygen) does not fully recapitulate exposure to intratumoral hypoxia (Godet et al., 2019). In this study, we sought to investigate whether chronic exposure to hypoxia in vitro (10 days at 1% oxygen) would better mimic the transcriptional effects of intratumoral hypoxia.
2023-09-01 | GSE240211 | GEO
Project description:Pancreatic cancer is a devastating and intractable disease with highly lethal rate, which is equal to incidence of the disease.It is well established that tumor microenvironment plays a pivotal role in tumor progression and metastasis.Tumor-associated macrophages (TAMs) are frequently found in close proximity with pancreatic cancer cells, but it is uncertain whether they are involved in pancreatic cancer progression.TAMs around the cancer regions usually exert their tumor-supporting functions by the secretion of cytokines and inflammatory mediators.In this study, we aim to investigate that whether tumor-associated macrophages regulate the gene expression profiles of pancreatic cancer cells both under normoxia and hypoxia.
2018-05-07 | GSE109110 | GEO
Project description:Systemic arterial smooth muscle cells are exposed to a broad range of oxygen concentrations under physiological conditions. Hypoxia can modulate the proliferative response of smooth muscle cells leading to speculation about its role in vasculogenesis, vascular remodelling and the pathogenesis of arterial disease. The effect of hypoxia has been inconsistent, however, with both enhanced proliferation and growth arrest reported. Nevertheless, these reports support an important effect of hypoxia on smooth muscle cell proliferation and, given its physiological and clinical relevance, this requires clarification. We posited that variation in O2 concentration, within the range that exists in vivo, may have different effects on the proliferation and survival of vascular smooth muscle cells. Keywords: expression profiles of hypoxia (1% and 3%) in HASMC
2007-12-11 | GSE4725 | GEO
Project description:Ischemia exists in many diseased tissues including arthritic joints, atherosclerotic plaques and malignant tumors. Macrophages accumulate in these sites and upregulate genes in response to the hypoxia present. We used microarrays to detail the hypoxia upregulated gene in human primary macrophages. Experiment Overall Design: Primary macrophages were differentiated for 7 days in vitro from human peripheral blood (monocyte-derived macrophages, MDMs) and were subjected to severe hypoxia (< 0.5% O2) or normoxia (20.9% O2) in 5% CO2 humidified multi-gas incubators.
2009-05-11 | E-GEOD-15949 | biostudies-arrayexpress
Project description:Macrophages are effector immune cells that experience substantial changes to oxygenation when transiting through tissues, especially when entering tumors or infected wounds. How hypoxia alters gene expression and macrophage effector function at the post-transcriptional level remains poorly understood. Here we use TimeLapse-seq to measure how inflammatory activation modifies the hypoxic response in primary macrophages. Nucleoside recoding sequencing allows derivation of steady-state transcript levels, degradation rates, and transcriptional synthesis rates from the same dataset. We find that hypoxia produces distinct responses from resting and inflammatory macrophages. Hypoxia induces destabilization of mRNA transcripts, though inflammatory macrophages substantially increase mRNA degradation compared to resting macrophages. Increased RNA turnover results in upregulation of ribosomal protein genes and downregulation of extracellular matrix components in inflammatory macrophages. Hypoxia induces gene expression changes similar to tumorigenic macrophages in solid tumor biopsies, including increased ribosomal protein expression, implying that post-transcriptional control contributes to translation regulation in tumorigenic macrophages.
2024-07-02 | GSE245750 | GEO