ArticleCellular and molecular life sciences : CMLS2012
NFκB and HIF display synergistic behaviour during hypoxic inflammation.
Article in Cellular and molecular life sciences : CMLS, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed.
- Hypoxia as an amplifier of synovial inflammation in rheumatoid arthritis.Nature reviews. Rheumatology · 2026Review
- The role of cyclooxygenase-2 in oxidative stress and inflammation: Implications for poultry health and production.Poultry science · 2026Review
- Exploring the neuroprotective potential of ligustrazine: a preclinical meta-analysis and machine learning perspective on cerebral ischemia-reperfusion injury.Frontiers in neuroscience · 2026Review
- The Role of Prostaglandins as Major Inflammatory Mediators in Colorectal Cancer.International journal of molecular sciences · 2025Review
- Modulation of hypoxia-inducible factor-1 signaling pathways in cancer angiogenesis, invasion, and metastasis by natural compounds: a comprehensive and critical review.Cancer metastasis reviews · 2024Review
- Suppression of NASH-Related HCC by Farnesyltransferase Inhibitor through Inhibition of Inflammation and Hypoxia-Inducible Factor-1α Expression.International journal of molecular sciences · 2023Article
- Cyclooxygenase‑2 contributes to the hypoxia‑induced aggravation of the neuroinflammation response stimulated by lipopolysaccharide in microglia.Experimental and therapeutic medicine · 2023Article
- Expression of placental glycans and its role in regulating peripheral blood NK cells during preeclampsia: a perspective.Frontiers in endocrinology · 2023Review
- Targeting HIF-1α by Natural and Synthetic Compounds: A Promising Approach for Anti-Cancer Therapeutics Development.Molecules (Basel, Switzerland) · 2022Review
- Mitochondrial Dysfunction and Oxidative Stress in Rheumatoid Arthritis.Antioxidants (Basel, Switzerland) · 2022Review
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- Skeletal Muscle in Hypoxia and Inflammation: Insights on the COVID-19 Pandemic.Frontiers in nutrition · 2022Review
- Potential role of mitochondria in gastric cancer detection: Fission and glycolysis.Oncology letters · 2021Review
- Metabolic reprogramming as a key regulator in the pathogenesis of rheumatoid arthritis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020Review
- Transcription Factors Regulation in Human Peripheral White Blood Cells during Hypobaric Hypoxia Exposure: an in-vivo experimental study.Scientific reports · 2019Article
- Regulation of Fibroblast Growth Factor 23 by Iron, EPO, and HIF.Current molecular biology reports · 2019Article
- Consequences of Hypoxia for the Pulmonary Alveolar Epithelial Cell Innate Immune Response.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Hypoxia-induced the upregulation of stromal cell-derived factor 1 in fibroblast-like synoviocytes contributes to migration of monocytes into synovium tissue in rheumatoid arthritis.Cell & bioscience · 2018Article
- Effects of Hypoxia and Bed Rest on Markers of Cardiometabolic Risk: Compensatory Changes in Circulating TRAIL and Glutathione Redox Capacity.Frontiers in physiology · 2018Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The oxygen-sensitive transcription factor hypoxia inducible factor (HIF) is a key regulator of gene expression during adaptation to hypoxia. Crucially, inflamed tissue often displays regions of prominent hypoxia. Recent studies have shown HIF signalling is intricately linked to that of the pro-inflammatory transcription factor nuclear factor kappa B (NFκB) during hypoxic inflammation. We describe the relative temporal contributions of each to hypoxia-induced inflammatory gene expression and investigate the level of crosstalk between the two pathways using a novel Gaussia princeps luciferase (Gluc) reporter system. Under the control of an active promoter, Gluc is expressed and secreted into the cell culture media, where it can be sampled and measured over time. Thus, Gluc constructs under the control of either HIF or NFκB were used to resolve their temporal transcriptional dynamics in response to hypoxia and to cytokine stimuli, respectively. We also investigated the interactions between HIF and NFκB activities using a construct containing the sequence from the promoter of the inflammatory gene cyclooxygenase 2 (COX-2), which includes functionally active binding sites for both HIF and NFκB. Finally, based on our experimental data, we constructed a mathematical model of the binding affinities of HIF and NFκB to their respective response elements to analyse transcriptional crosstalk. Taken together, these data reveal distinct temporal HIF and NFκB transcriptional activities in response to hypoxic inflammation. Furthermore, we demonstrate synergistic activity between these two transcription factors on the regulation of the COX-2 promoter, implicating a co-ordinated role for both HIF and NFκB in the expression of COX-2 in hypoxic inflammation.
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