ArticleImmunology1999
Regulation of macrophage inflammatory protein-2 gene expression by oxidative stress in rat alveolar macrophages.
Article in Immunology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- The global contribution of outdoor air pollution to the incidence, prevalence, mortality and hospital admission for chronic obstructive pulmonary disease: a systematic review and meta-analysis.International journal of environmental research and public health · 2014Pooled it
- ISM1 suppresses LPS-induced acute lung injury and post-injury lung fibrosis in mice.Molecular medicine (Cambridge, Mass.) · 2022Article
- Molecular Mechanism of Aniline Induced Spleen Toxicity and Neuron Toxicity in Experimental Rat Exposure: A Review.Current neuropharmacology · 2019Review
- Long-range function of secreted small nucleolar RNAs that direct 2'-The Journal of biological chemistry · 2018Article
- Hydrogen Peroxide: A Potential Wound Therapeutic Target?Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2017Review
- Aquaporin-3 potentiates allergic airway inflammation in ovalbumin-induced murine asthma.Scientific reports · 2016Article
- TNF-α induces CXCL1 chemokine expression and release in human vascular endothelial cells in vitro via two distinct signaling pathways.Acta pharmacologica Sinica · 2014Article
- Transcriptional regulation of CXC-ELR chemokines KC and MIP-2 in mouse pancreatic acini.American journal of physiology. Gastrointestinal and liver physiology · 2010Article
- Rtp801, a suppressor of mTOR signaling, is an essential mediator of cigarette smoke-induced pulmonary injury and emphysema.Nature medicine · 2010Article
- Activation of oxidative stress-responsive signaling pathways in early splenotoxic response of aniline.Toxicology and applied pharmacology · 2008Article
- Regulation of MUC5AC expression by NAD(P)H:quinone oxidoreductase 1.Free radical biology & medicine · 2007Article
- Molecular mechanisms of interleukin-10-mediated inhibition of NF-kappaB activity: a role for p50.Clinical and experimental immunology · 2004Article
- Fine tuning the transcriptional regulation of the CXCL1 chemokine.Progress in nucleic acid research and molecular biology · 2003Review
- Down-regulation of glycosylphosphatidylinositol-specific phospholipase D induced by lipopolysaccharide and oxidative stress in the murine monocyte- macrophage cell line RAW 264.7.Infection and immunity · 2001Article
- Regulation of chemokine mRNA expression in a rat model of vanadium-induced pulmonary inflammation.Inflammation · 2000Article
- Expression and regulation of macrophage inflammatory protein-2 gene by vanadium in mouse macrophages.Inflammation · 2000Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Chemokines are important mediators in the development of inflammation. Our previous work demonstrated that an oxidative stress can up-regulate mRNA expression of a CC chemokine macrophage inflammatory protein (MIP)-1alpha in rat alveolar macrophages. In the present study, we further investigate whether an oxidative stress can regulate the gene expression of a related CXC chemokine MIP-2, involved in both neutrophil chemotaxis and activation. A rat alveolar macrophage cell line (NR8383) was exposed to 10 microg/ml bacterial lipopolysaccharide (LPS) and MIP-2 mRNA levels dramatically increased after 4 hr of stimulation. This increase by LPS was attenuated by co-treatment with the antioxidants N-acetylcysteine and dimethylsulphoxide, suggesting that the induction of MIP-2 mRNA is mediated via the generation of reactive oxygen species. To assess directly the role of oxidative stress on regulation of MIP-2 mRNA expression, macrophages were exposed to H2O2. MIP-2 mRNA levels had significantly increased after 1 hr exposure to 0.5 mm H2O2, were maximally increased after 4 hr and decreased after 6 hr. Co-treatment of macrophages with the transcriptional inhibitor actinomycin D eliminated the H2O2-induction of MIP-2 mRNA, implicating a role for transcriptional activation in increased expression of MIP-2. Genomic cloning of the rat MIP-2 gene 5'-flanking region has identified a consensus nuclear factor-kappaB (NF-kappaB) binding site. Gel-mobility shift assays revealed NF-kappaB binding to the MIP-2 promoter/enhancer sequence was induced by H2O2. LPS treatment for 4 hr also significantly activated NF-kappaB binding, which could also be attenuated by pretreatment with N-acetylcysteine at the doses that reduced MIP-2 mRNA expression. The half-life of MIP-2 mRNA transcripts was also increased by H2O2 treatment. These observations indicate that MIP-2 gene expression is subject to both transcriptional and post-transcriptional control in response to an H2O2 oxidative stress.
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