ArticleProceedings of the National Academy of Sciences of the United States of America1997
Inflammatory mediators are perpetuated in macrophages resistant to apoptosis induced by hypoxia.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 59 citations in OpenAlex.
- Fructose induces inflammatory activation in macrophages and microglia through the nutrient-sensing ghrelin receptor.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Combined assessment of inflammation and food intake contributes to prognostic stratification of gastric cancer.Frontiers in oncology · 2025Article
- Development of a Redox-Polymer-Based Electrochemical Glucose Biosensor Suitable for Integration in Microfluidic 3D Cell Culture Systems.Biosensors · 2023Article
- Differential expression of checkpoint markers in the normoxic and hypoxic microenvironment of glioblastomas.Brain pathology (Zurich, Switzerland) · 2023Article
- Bovine milk exosomes affected proliferation of macrophages under hypoxia.Current research in food science · 2022Article
- Systemic Immune-Inflammation Index Predicts Overall Survival in Patients with Gastric Cancer: a Propensity Score-Matched Analysis.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2021Article
- Local Stabilization of Hypoxia-Inducible Factor-1α Controls Intestinal InflammationFrontiers in immunology · 2020Article
- Cellular Stress Responses and Gut Microbiota in Inflammatory Bowel Disease.Gastroenterology research and practice · 2018Review
- Intestinal hypoxia and hypoxia-induced signalling as therapeutic targets for IBD.Nature reviews. Gastroenterology & hepatology · 2017Review
- Hsp70 and HSF-1 expression is altered in the tissues of pigs transported for various periods of times.Journal of veterinary science · 2012Article
- Hypoxia enhances the proliferative response of macrophages to CSF-1 and their pro-survival response to TNF.PloS one · 2012Article
- Molecular mechanisms regulating macrophage response to hypoxia.Frontiers in immunology · 2011Article
- Role of Pluronic block copolymers in modulation of heat shock protein 70 expression.International journal of hyperthermia : the official journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group · 2011Article
- Genetic variations in HSPA8 gene associated with coronary heart disease risk in a Chinese population.PloS one · 2010Article
- Hypoxia skews dendritic cells to a T helper type 2-stimulating phenotype and promotes tumour cell migration by dendritic cell-derived osteopontin.Immunology · 2009Article
- Hypoxia. Hypoxia, hypoxia inducible factor and myeloid cell function.Arthritis research & therapy · 2009Review
- Multiplex bead analysis of vitreous and serum concentrations of inflammatory and proangiogenic factors in diabetic patients.Molecular vision · 2008Article
- Effect of high-fat enteral nutrition on hepatocyte injury in response to hemorrhagic shock in the rat.World journal of surgery · 2007Article
- Heat-shocked monocytes are resistant to Staphylococcus aureus-induced apoptotic DNA fragmentation due to expression of HSP72.Infection and immunity · 1999Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A hypoxic/anoxic microenvironment has been proposed to exist within a vascular lesion due to intimal or medial cell proliferation in vascular diseases. Here, we examined whether hypoxia alters macrophage function by exposing murine macrophage-like RAW 264.7 (RAW) cells to hypoxia (2% O2). When cells were exposed to hypoxia, a significant number of RAW cells underwent apoptosis. Additionally, small subpopulations of RAW cells were resistant to hypoxia-induced apoptosis. Through repeated cycles of hypoxia exposure, hypoxia-induced apoptosis-resistant macrophages (HARMs) were selected; HARM cells demonstrate >70% resistance to hypoxia-induced apoptosis, as compared with the parental RAW cells. When heat shock protein (HSP) expression was examined after hypoxia, we observed a significant decrease in constitutive heat shock protein 70 (HSC 70) in RAW cells, but not in HARMs, as compared with the control normoxic condition (21% O2). In contrast, the expression level of glucose-regulated protein 78 (GRP 78) in RAW and HARM cells after hypoxia treatment was not altered, suggesting that HSC 70 and not GRP 78 may play a role in protection against hypoxia-induced apoptosis. When tumor necrosis factor alpha (TNF-alpha) production was examined after hypoxic treatment, a significant increase in TNF-alpha production in HARM but decrease in RAW was observed, as compared with cells cultured in normoxic conditions. HARM cells also exhibit a much lower level of modified-LDL uptake than do RAW cells, suggesting that HARMs may not transform into foam cells. These results suggest that a selective population of macrophages may adapt to potentially pathological hypoxic conditions by overcoming the apoptotic signal.
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