scholarly journals Stretch-activated signaling pathways responsible for early response gene expression in fetal lung epithelial cells

2006 ◽  
Vol 210 (1) ◽  
pp. 133-143 ◽  
Author(s):  
Ian B. Copland ◽  
Martin Post
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Signaling Pathways ◽  
Fetal Lung ◽  
Early Response ◽  
Lung Epithelial Cells ◽  
Response Gene ◽  
Early Response Gene ◽  
Lung Epithelial

Liposome-mediated transfection of fetal lung epithelial cells: DNA degradation and enhanced superoxide toxicity

1998 ◽  
Vol 275 (3) ◽  
pp. L452-L460 ◽  
Author(s):  
A. Keith Tanswell ◽  
Olivier Staub ◽  
Richard Iles ◽  
Rosetta Belcastro ◽  
Judy Cabacungan ◽  
...  
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Reporter Gene ◽  
Fetal Lung ◽  
Reporter Gene Expression ◽  
Lung Epithelial Cells ◽  
Dna Uptake ◽  
Exogenous Dna ◽  
Lipid Ratio ◽  
Lung Epithelial

Cationic liposomes, 1:1 (mol/mol) 1,2-dioleoyldimethylammonium chloride-1,2-dioleoyl- sn-glycero-3-phosphoethanolamine, were used to transfect primary cultures of distal rat fetal lung epithelial cells with pCMV4-based plasmids. A DNA-to-lipid ratio of 1:10 to 1:15 (wt/wt) optimized DNA uptake over a 24-h exposure. At a fixed DNA-to-lipid ratio of 1:15, chloramphenicol acetyltransferase (CAT) reporter gene expression declined at lipid concentrations > 2.5 nmol/cm2 cell surface area, whereas DNA uptake remained concentration dependent. CAT expression peaked 48 h after removal of the liposome-DNA complex, declining thereafter. Reporter gene expression was increased, and supercoiled cDNA degradation was reduced by the addition of 0.2 mM nicotinamide and 10 μM chloroquine. Rat fetal lung epithelial cells transfected with two different expression cassettes had an increased susceptibility to superoxide-mediated cytotoxicity. This could be attributed to a nonspecific delivery of exogenous DNA or some other copurified factor. The DNA-dependent increase in superoxide-mediated cytotoxicity, but not basal levels of cytotoxicity, was inhibited by the addition of 0.2 mM nicotinamide and 10 μM chloroquine.

scholarly journals Differential induction of c-fos, c-jun, and apoptosis in lung epithelial cells exposed to ROS or RNS

1997 ◽  
Vol 273 (4) ◽  
pp. L789-L796 ◽  
Author(s):  
Yvonne M. W. Janssen ◽  
Sadis Matalon ◽  
Brooke T. Mossman
Keyword(s):  
Epithelial Cells ◽  
Early Response ◽  
Lung Epithelial Cells ◽  
Mrna Levels ◽  
Activator Protein 1 ◽  
Recognition Sequence ◽  
Response Gene ◽  
End Points ◽  
Lung Epithelial ◽  
Phenotypic Responses

Reactive oxygen (ROS) or nitrogen (RNS) species can affect epithelial cells to cause acute damage and an array of pulmonary diseases. The goal of this study was to determine patterns of early response gene expression and functional end points of exposure to nitric oxide (NO ⋅), H2O2, or peroxynitrite (ONOO−) in a line of rat lung epithelial (RLE) cells. Our focus was on c- fos and c- jun protooncogenes, as these genes play an important role in proliferation or apoptosis, possible end points of exposure to reactive metabolites in lung. Our data demonstrate that NO ⋅ generated by spermine 1,3-propanediamine N-{4-[1-(3-aminopropyl)-2-hydroxy-2-nitrosohydrazino]butyl} or S-nitroso- N-acetylpenicillamine as well as H2O2cause increased c- fos and c- jun mRNA levels, nuclear proteins, and complexes binding the activator protein-1 recognition sequence in RLE cells. These agents also lead to apoptosis and increased membrane permeability. In contrast, exogenously administered ONOO− or 3-morpholinosydnonimine do not induce protooncogenes or apoptosis in RLE cells despite nitration of tyrosines. We conclude that ROS and RNS can elicit distinct molecular and phenotypic responses in a target cell of pulmonary disease.

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
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