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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
4 Pt 1
|
| pubmed:dateCreated |
1998-11-23
|
| pubmed:abstractText |
Cultured rat fetal distal lung epithelial cells (FDLEs), when switched from fetal (3%) to postnatal (21%) O2 concentrations, have increased epithelial Na+ channel (ENaC) mRNA levels and amiloride-sensitive Na+ transport [O. Pitkänen, A. K. Tanswell, G. Downey, and H. O'Brodovich. Am. J. Physiol. 270 (Lung Cell. Mol. Physiol. 14): L1060-L1066, 1996]. The mechanisms by which O2 mediates these effects are unknown. After isolation, FDLEs were kept at 3% O2 overnight, then switched to 21% O2 (3-21% O2 group) or maintained at 3% O2 (3-3% O2 group) for 48 h. The amiloride-sensitive short-circuit current (Isc) in the 3-21% O2 group was double that in the 3-3% O2 group. Amiloride-sensitive Isc could not be induced by medium conditioned by 21% O2-exposed FDLEs but was reversed by returning the cells to 3% O2. Neither the cyclooxygenase inhibitor ibuprofen, liposome-encapsulated catalase, nor hydroperoxide scavengers (U-74389G or Trolox) blocked the O2-induced amiloride-sensitive Isc. In contrast, the cell-permeable superoxide scavenger tetramethylpiperidine-N-oxyl (TEMPO) eliminated the O2-induced increases in amiloride-sensitive Isc and ENaC mRNA levels. The switch from 3 to 21% O2 induced the transcription factor nuclear factor-kappaB, which could also be blocked by TEMPO. We conclude that 1) the O2-induced increase in amiloride-sensitive Isc is reversible and 2) the O2-induced increase in amiloride-sensitive Isc and ENaC mRNA levels is associated with activation of nuclear factor-kappaB and may be mediated, at least in part, by superoxide.
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| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Amiloride,
http://linkedlifedata.com/resource/pubmed/chemical/Free Radical Scavengers,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/Oligodeoxyribonucleotides,
http://linkedlifedata.com/resource/pubmed/chemical/Oxygen,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Superoxides,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factor AP-1
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Oct
|
| pubmed:issn |
0002-9513
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
275
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
L764-70
|
| pubmed:dateRevised |
2010-5-13
|
| pubmed:meshHeading |
pubmed-meshheading:9755109-Amiloride,
pubmed-meshheading:9755109-Animals,
pubmed-meshheading:9755109-Base Sequence,
pubmed-meshheading:9755109-Binding Sites,
pubmed-meshheading:9755109-Cells, Cultured,
pubmed-meshheading:9755109-Consensus Sequence,
pubmed-meshheading:9755109-Embryo, Mammalian,
pubmed-meshheading:9755109-Epithelial Cells,
pubmed-meshheading:9755109-Free Radical Scavengers,
pubmed-meshheading:9755109-Gene Expression Regulation,
pubmed-meshheading:9755109-Hyperoxia,
pubmed-meshheading:9755109-Lung,
pubmed-meshheading:9755109-NF-kappa B,
pubmed-meshheading:9755109-Oligodeoxyribonucleotides,
pubmed-meshheading:9755109-Oxygen,
pubmed-meshheading:9755109-Rats,
pubmed-meshheading:9755109-Rats, Wistar,
pubmed-meshheading:9755109-Sodium Channels,
pubmed-meshheading:9755109-Superoxides,
pubmed-meshheading:9755109-Transcription Factor AP-1
|
| pubmed:year |
1998
|
| pubmed:articleTitle |
O2-induced ENaC expression is associated with NF-kappaB activation and blocked by superoxide scavenger.
|
| pubmed:affiliation |
Medical Research Council Group in Lung Development, Hospital for Sick Children Research Institute and Department of Paediatrics, University of Toronto, Toronto, Ontario, Canada M5G 1X8.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|