scholarly journals Cu,Zn–Superoxide Dismutase–Mediated Redox Regulation of Jumonji Domain Containing 3 Modulates Macrophage Polarization and Pulmonary Fibrosis

2016 ◽  
Vol 55 (1) ◽  
pp. 58-71 ◽  
Author(s):  
Chao He ◽  
Jennifer L. Larson-Casey ◽  
Linlin Gu ◽  
Alan J. Ryan ◽  
Shubha Murthy ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Pulmonary Fibrosis ◽  
Redox Regulation ◽  
Macrophage Polarization

Modern Concepts on the Role of Inflammation in Pulmonary Fibrosis

2011 ◽  
Vol 135 (6) ◽  
pp. 780-788 ◽  
Author(s):  
Robert J. Homer ◽  
Jack A. Elias ◽  
Chun Gun Lee ◽  
Erica Herzog
Keyword(s):  
Cell Death ◽  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Therapeutic Intervention ◽  
Macrophage Polarization ◽  
Critical Evaluation ◽  
Clinical Context ◽  
Disease Biomarkers ◽  
Unpublished Research

Abstract Context.—Idiopathic pulmonary fibrosis is a uniformly lethal disease with limited biomarkers and no proven therapeutic intervention short of lung transplantation. Pulmonary fibrosis at one time was thought to be a result of inflammation in the lung. Although some forms of pulmonary fibrosis may result from inflammation, idiopathic pulmonary fibrosis is currently thought to result from cell death primarily and inflammation secondarily. Objective.—To determine the role of inflammation in pulmonary fibrosis in light of our laboratory's published and unpublished research and published literature. Data Sources.—Review based on our laboratory's published and unpublished experimental data with relevant background and clinical context provided. Conclusions.—Although cell death is central to pulmonary fibrosis, the proper cytokine environment leading to macrophage polarization is also critical. Evaluation of this environment is promising both for the development of disease biomarkers and for targets for therapeutic intervention.

scholarly journals Copper–zinc superoxide dismutase-mediated redox regulation of bortezomib resistance in multiple myeloma

Redox Biology ◽  
2015 ◽  
Vol 4 ◽  
pp. 23-33 ◽  
Author(s):  
Kelley Salem ◽  
Michael L. McCormick ◽  
Erik Wendlandt ◽  
Fenghuang Zhan ◽  
Apollina Goel
Keyword(s):  
Multiple Myeloma ◽  
Superoxide Dismutase ◽  
Redox Regulation ◽  
Copper Zinc Superoxide Dismutase ◽  
Zinc Superoxide Dismutase ◽  
Copper Zinc

Elevated Serum Superoxide Dismutase Levels Correlate with Disease Severity and Neutrophil Degranulation in Idiopathic Pulmonary Fibrosis

1993 ◽  
Vol 85 (3) ◽  
pp. 353-359 ◽  
Author(s):  
Rosa Maria Borzì ◽  
Brunella Grigolo ◽  
R. Meliconi ◽  
L. Fasano ◽  
C. Sturani ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Disease Severity ◽  
Tissue Damage ◽  
Elevated Serum ◽  
Polymorphonuclear Cell ◽  
Control Subjects ◽  
Neutrophil Degranulation ◽  
Severity Indexes

1. Tissue damage in idiopathic pulmonary fibrosis is due in part to oxidant-antioxidant imbalance. 2. We evaluated the serum levels of the antioxidant enzyme Cu/Zn superoxide dismutase (EC 1.15.1.1) in 25 patients with idiopathic pulmonary fibrosis, 34 patients with sarcoidosis and 40 healthy control subjects by an enzyme immunometric assay. 3. We found that patients with idiopathic pulmonary fibrosis have higher serum Cu/Zn superoxide dismutase levels than control subjects and patients with sarcoidosis. In addition, serum Cu/Zn superoxide dismutase levels correlate with disease severity indexes in patients with idiopathic pulmonary fibrosis. 4. The increase in serum Cu/Zn superoxide dismutase level in idiopathic pulmonary fibrosis could depend on degranulation of activated neutrophils or release from damaged cells. To elucidate the contribution of neutrophil degranulation we determined the polymorphonuclear cell elastase level in the same specimens. We found a strong correlation between serum Cu/Zn superoxide dismutase and polymorphonuclear cell elastase activities, and, in patients with idiopathic pulmonary fibrosis, we observed higher levels of polymorphonuclear cell elastase than in control subjects and patients with sarcoidosis, which correlated positively with disease severity indexes. 5. Cu/Zn superoxide dismutase can catalyse the dismutation of O2 into H2Oz and generate OH · These oxygen radicals are probably the major factors responsible for tissue damage (in particular, alveolar and endothelial cells) and fibrosis in experimental lung injury. 6. Taking into account: (a) the specific enzymic activity of Cu/Zn superoxide dismutase (i.e. production of H2O2 and OH ·), (b) the possible enhancement of the effect of reduced glutathione deficiency (high H2O2) by increased Cu/Zn superoxide dismutase activity, and (c) the correlation that we found between disease severity and Cu/Zn superoxide dismutase and polyphorphonuclear cell elastase levels, we suggest that, in idiopathic pulmonary fibrosis, increased activities of Cu/Zn superoxide dismutase and polymorphonuclear cell elastase can achieve a pro-inflammatory pathogenic effect. 7. However, the results of this study of serum Cu/Zn superoxide dismutase and polymorphonuclear cell elastase concentrations in individual patients does not support a clear-cut cause-effect relationship between these enzyme levels and the clinical changes in the patients.

scholarly journals Redox Regulation of Adenovirus-Induced AP-1 Activation by Overexpression of Manganese-Containing Superoxide Dismutase

2002 ◽  
Vol 76 (1) ◽  
pp. 355-363 ◽  
Author(s):  
Hannah J. Zhang ◽  
Victoria J. Drake ◽  
Linjing Xu ◽  
Jianfang Hu ◽  
Frederick E. Domann ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Dna Binding ◽  
Redox Regulation ◽  
Recombinant Adenovirus ◽  
Redox Status ◽  
Binding Activity ◽  
Dna Binding Activity ◽  
Promising Tool ◽  
Gel Shift Assay ◽  
Intracellular Redox Status

ABSTRACT Adenovirus gene therapy is a promising tool in the clinical treatment of many genetic and acquired diseases. However, it has also caused pathogenic effects in organs such as the liver. The redox-sensitive transcription factors AP-1 and NF-κB have been implicated in these effects. To study the mechanisms of adenovirus-mediated AP-1 and NF-κB activation and the possible involvement of oxidative stress in adenovirus transduction, rats were injected with either replication-defective recombinant adenovirus with DNA containing the cytomegalovirus promoter region only (AdCMV), adenovirus containing human manganese-containing superoxide dismutase (MnSOD) cDNA (AdMnSOD), or vehicle. Compared to vehicle and AdCMV transduction, MnSOD gene transfer yielded a fivefold increase in liver MnSOD activity 7 days postinjection. Gel shift assay showed that AdCMV transduction induced DNA binding activity for AP-1 but not NF-κB. MnSOD overexpression abolished this activation. Western blotting analysis of c-Fos and c-Jun suggested that up-regulation of c-fos and c-jun gene expression does not directly contribute to the induction of AP-1 activation. Glutathione/glutathione disulfide ratios were decreased by adenovirus transduction and restored by MnSOD overexpression. The AP-1 binding activity that was induced by AdCMV was decreased by immunoprecipitation of Ref-1 protein. Ref-1 involvement was confirmed by restoration of AP-1 binding activity after the immunoprecipitated Ref-1 protein had been added back. AP-1 DNA binding activity was also elevated in control and AdMnSOD-injected rats after addition of the immunoprecipitated Ref-1 protein. These data indicate that cellular transduction by recombinant adenovirus stimulates AP-1 DNA binding activity. Furthermore, our results suggest that MnSOD overexpression decreases AP-1 DNA binding activity by regulating intracellular redox status, with the possible involvement of Ref-1 in this redox-sensitive pathway.

Role of extracellular superoxide dismutase in bleomycin-induced pulmonary fibrosis

2002 ◽  
Vol 282 (4) ◽  
pp. L719-L726 ◽  
Author(s):  
Russell P. Bowler ◽  
Mike Nicks ◽  
Karrie Warnick ◽  
James D. Crapo
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Pulmonary Fibrosis ◽  
Lung Injury ◽  
Immunohistochemical Staining ◽  
Extracellular Superoxide Dismutase ◽  
Wild Type ◽  
Injured Lung ◽  
Intracellular Oxidative Stress

Bleomycin administration results in well-described intracellular oxidative stress that can lead to pulmonary fibrosis. The role of alveolar interstitial antioxidants in this model is unknown. Extracellular superoxide dismutase (EC-SOD) is the primary endogenous extracellular antioxidant enzyme and is abundant in the lung. We hypothesized that EC-SOD plays an important role in attenuating bleomycin-induced lung injury. Two weeks after intratracheal bleomycin administration, we found that wild-type mice induced a 106 ± 25% increase in lung EC-SOD. Immunohistochemical staining revealed that a large increase in EC-SOD occurred in injured lung. Using mice that overexpress EC-SOD specifically in the lung, we found a 53 ± 14% reduction in bleomycin-induced lung injury assessed histologically and a 17 ± 6% reduction in lung collagen content 2 wk after bleomycin administration. We conclude that EC-SOD plays an important role in reducing the magnitude of lung injury from extracellular free radicals after bleomycin administration.

Redox Regulation of the Macrophage Phenotype Modulates Pulmonary Fibrosis

2012 ◽  
Vol 53 ◽  
pp. S55
Author(s):  
Chao He ◽  
Alan James Ryan ◽  
Shubha Murthy ◽  
A. Brent Carter
Keyword(s):  
Pulmonary Fibrosis ◽  
Redox Regulation ◽  
Macrophage Phenotype

scholarly journals Defense Responses of Wheat Seedling under Biotic Stress Mimicked by the Linear β-(1,3)-Glucan

2020 ◽  
pp. 13-23
Author(s):  
Abderrakib Zahid
Keyword(s):  
Reactive Oxygen Species ◽  
Superoxide Dismutase ◽  
Antioxidant System ◽  
Biotic Stress ◽  
Redox Regulation ◽  
Wheat Seedling ◽  
Defense Responses ◽  
Ros Production ◽  
Oxygen Species ◽  
Detoxification Mechanisms

Reactive oxygen species (ROS) production causes damage, and to better deal with the toxic effects of ROS, the seeds have developed detoxification mechanisms, among which the enzymes of the antioxidant system (catalase, superoxide dismutase, ascorbate peroxidase). Another result supports the link between ROS and redox regulation catalyzed by redoxin family in the seed. Among which, thioredoxins (Trxs) and peroxiredoxins (Prxs), particularly 1-Cys-Prx, expressed during maturation and germination steps.

scholarly journals Roles of Macrophage Polarization and Macrophage-Derived miRNAs in Pulmonary Fibrosis

2021 ◽  
Vol 12 ◽  
Author(s):  
Amit Kishore ◽  
Martin Petrek
Keyword(s):  
Pulmonary Fibrosis ◽  
Tissue Injury ◽  
Macrophage Polarization ◽  
Future Perspective ◽  
Current Evidence ◽  
M2 Macrophage ◽  
Cellular Mirnas ◽  
Exosomal Mirnas ◽  
Macrophage Populations ◽  
And Function

This mini-review summarizes the current evidence for the role of macrophage activation and polarization in inflammation and immune response pertinent to interstitial lung disease, specifically pulmonary fibrosis. In the fibrosing lung, the production and function of inflammatory and fibrogenic mediators involved in the disease development have been reported to be regulated by the effects of polarized M1/M2 macrophage populations. The M1 and M2 macrophage phenotypes were suggested to correspond with the pro-inflammatory and pro-fibrogenic signatures, respectively. These responses towards tissue injury followed by the development and progression of lung fibrosis are further regulated by macrophage-derived microRNAs (miRNAs). Besides cellular miRNAs, extracellular exosomal-miRNAs derived from M2 macrophages have also been proposed to promote the progression of pulmonary fibrosis. In a future perspective, harnessing the noncoding miRNAs with a key role in the macrophage polarization is, therefore, suggested as a promising therapeutic strategy for this debilitating disease.

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