Hypoxic Modulation of Manganese Superoxide Dismutase Promoter Activity and Gene Expression in Lung Epithelial Cells

1999 ◽  
Vol 21 (1) ◽  
pp. 119-127 ◽  
Author(s):  
Tauni Ohman ◽  
Gregory Parish ◽  
Robert M. Jackson
Keyword(s):  
Gene Expression ◽  
Superoxide Dismutase ◽  
Epithelial Cells ◽  
Promoter Activity ◽  
Manganese Superoxide Dismutase ◽  
Lung Epithelial Cells ◽  
Manganese Superoxide ◽  
Lung Epithelial

Overexpression of Manganese Superoxide Dismutase Protects Lung Epithelial Cells against Oxidant Injury

2001 ◽  
Vol 24 (4) ◽  
pp. 436-441 ◽  
Author(s):  
Anatoliy M. Ilizarov ◽  
Hshi-Chi Koo ◽  
Jeffrey A. Kazzaz ◽  
Lin L. Mantell ◽  
Yuchi Li ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Epithelial Cells ◽  
Manganese Superoxide Dismutase ◽  
Lung Epithelial Cells ◽  
Oxidant Injury ◽  
Manganese Superoxide ◽  
Lung Epithelial

Nitric oxide increases IL-8 gene transcription and mRNA stability to enhance IL-8 gene expression in lung epithelial cells

2004 ◽  
Vol 287 (4) ◽  
pp. L764-L773 ◽  
Author(s):  
Loretta Sparkman ◽  
Vijayakumar Boggaram
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Protein Kinase ◽  
Epithelial Cells ◽  
Gene Transcription ◽  
Mrna Stability ◽  
Inflammatory Responses ◽  
Lung Epithelial Cells ◽  
Mrna Levels ◽  
Lung Epithelial

Interleukin (IL)-8, a C-X-C chemokine, is a potent chemoattractant and an activator for neutrophils, T cells, and other immune cells. The airway and respiratory epithelia play important roles in the initiation and modulation of inflammatory responses via production of cytokines and surfactant. The association between elevated levels of nitric oxide (NO) and IL-8 in acute lung injury associated with sepsis, acute respiratory distress syndrome, respiratory syncytial virus infection in infants, and other inflammatory diseases suggested that NO may play important roles in the control of IL-8 gene expression in the lung. We investigated the role of NO in the control of IL-8 gene expression in H441 lung epithelial cells. We found that a variety of NO donors significantly induced IL-8 mRNA levels, and the increase in IL-8 mRNA was associated with an increase in IL-8 protein. NO induction of IL-8 mRNA was due to increases in IL-8 gene transcription and mRNA stability. NO induction of IL-8 mRNA levels was not inhibited by 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one and KT-5823, inhibitors of soluble guanylate cyclase and protein kinase G, respectively, and 8-bromo-cGMP did not increase IL-8 mRNA levels. This indicated that NO induces IL-8 mRNA levels independently of changes in the intracellular cGMP levels. NO induction of IL-8 mRNA was significantly reduced by inhibitors of extracellular regulated kinase and protein kinase C. IL-8 induction by NO was also reduced by hydroxyl radical scavengers such as dimethyl sulfoxide and dimethylthiourea, indicating the involvement of hydroxyl radicals in the induction process. NO induction of IL-8 gene expression could be a significant contributing factor in the initiation and induction of inflammatory response in the respiratory epithelium.

scholarly journals Selective Up-regulation of Cytokine-induced RANTES Gene Expression in Lung Epithelial Cells by Overexpression of IκBR

1997 ◽  
Vol 272 (32) ◽  
pp. 20191-20197 ◽  
Author(s):  
Prabir Ray ◽  
Liyan Yang ◽  
Dong-Hong Zhang ◽  
Samir K. Ghosh ◽  
Anuradha Ray
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Lung Epithelial Cells ◽  
Lung Epithelial

scholarly journals Responses of A549 human lung epithelial cells to cristobalite and α-quartz exposures assessed by toxicoproteomics and gene expression analysis

2016 ◽  
Vol 37 (6) ◽  
pp. 721-731 ◽  
Author(s):  
Ngoc Q. Vuong ◽  
Patrick Goegan ◽  
Francesco De Rose ◽  
Dalibor Breznan ◽  
Errol M. Thomson ◽  
...  
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Expression Analysis ◽  
Gene Expression Analysis ◽  
Human Lung ◽  
Lung Epithelial Cells ◽  
Lung Epithelial ◽  
Human Lung Epithelial Cells

Mechanical strain mimicking breathing amplifies alterations in gene expression induced by SiO2 NPs in lung epithelial cells

2019 ◽  
Vol 13 (9) ◽  
pp. 1227-1243 ◽  
Author(s):  
Carmen Schmitz ◽  
Jennifer Welck ◽  
Isabella Tavernaro ◽  
Marianna Grinberg ◽  
Jörg Rahnenführer ◽  
...  
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Mechanical Strain ◽  
Lung Epithelial Cells ◽  
Lung Epithelial

Rat lung antioxidant enzymes: differences in perinatal gene expression and regulation

1992 ◽  
Vol 263 (4) ◽  
pp. L466-L470 ◽  
Author(s):  
L. B. Clerch ◽  
D. Massaro
Keyword(s):  
Gene Expression ◽  
Superoxide Dismutase ◽  
Antioxidant Enzymes ◽  
Manganese Superoxide Dismutase ◽  
Late Gestation ◽  
Postnatal Exposure ◽  
Sod Activity ◽  
Copper Zinc Superoxide Dismutase ◽  
Manganese Superoxide ◽  
Copper Zinc

The lung activity of the antioxidant enzymes (AOEs) copper, zinc superoxide dismutase (Cu,Zn SOD), catalase (CAT), and glutathione peroxidase (GP), but not manganese superoxide dismutase (Mn SOD), increases in rats during late gestation; the concentrations of Cu,Zn SOD mRNA and CAT mRNA also rise. During early postnatal exposure to > 95% O2, the lung activity of Cu,Zn SOD, CAT, and GP increases. We now show 1) the lung concentration of Mn SOD mRNA and GP mRNA does not increase in late gestation; 2) Mn SOD activity and the concentration of its mRNA and of GP mRNA increase during exposure of neonatal rats to > 95% O2; and 3) as previously shown for CAT mRNA, the increase in lung concentration of the mRNAs for Cu,Zn SOD, Mn SOD, and GP during early postnatal hyperoxia occurs with a 70–80% prolongation of the half-life of these mRNAs. We conclude that 1) in late gestation the level at which lung AOE gene expression is regulated differs among the enzymes, 2) the level at which lung AOE gene expression is regulated shortly after birth in response to > 95% O2 is uniform among the enzymes, and 3) the lung's AOE response to neonatal hyperoxia is not merely a step-up of its prenatal regulation but involves different regulatory mechanisms based on increased stability of AOE mRNAs

scholarly journals The NS1 Protein of Influenza A Virus Blocks RIG-I-Mediated Activation of the Noncanonical NF-κB Pathway and p52/RelB-Dependent Gene Expression in Lung Epithelial Cells

2012 ◽  
Vol 86 (18) ◽  
pp. 10211-10217 ◽  
Author(s):  
Andrea Rückle ◽  
Emanuel Haasbach ◽  
Ilkka Julkunen ◽  
Oliver Planz ◽  
Christina Ehrhardt ◽  
...  
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Influenza A Virus ◽  
Influenza A ◽  
Target Gene ◽  
Lung Epithelial Cells ◽  
Ns1 Protein ◽  
Antiviral Immune Response ◽  
Lung Epithelial ◽  
Infected Cells

Influenza A virus (IAV) infection of epithelial cells activates NF-κB transcription factors via the canonical NF-κB signaling pathway, which modulates both the antiviral immune response and viral replication. Since almost nothing is known so far about a function of noncanonical NF-κB signaling after IAV infection, we tested infected cells for activation of p52 and RelB. We show that the viral NS1 protein strongly inhibits RIG-I-mediated noncanonical NF-κB activation and expression of the noncanonical target gene CCL19.

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