| Mitogen-activated protein kinases mediate peroxynitrite-induced cell death in human bronchial epithelial cells. | |
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MedLine Citation:
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PMID: 12598225 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Peroxynitrite, formed by the reaction of nitric oxide (NO. ) with superoxide anions (O(2)(-).), may play a role in the pathophysiology of inflammation. The effects of 3-morpholinosydnonimine (SIN-1), a peroxynitrite generator, on the human bronchial epithelial cell line BEAS-2B, were examined. SIN-1 exposure resulted in cell death in a time- and dose-dependent manner. Depletion of intracellular glutathione increased the vulnerability of the cells. Pretreatment with Mn(III)tetrakis(N-methyl-4'-pyridyl)porphyrin (MnTMPyP) or hydroxocobalamin (HC), O(2)(-). and NO. scavengers, respectively, reduced significantly SIN-1-induced cell death (18.66 +/- 3.57 vs. 77.01 +/- 14.07 or 82.20 +/- 9.64, % cell viability SIN-1 vs. MnTMPyP or HC). Moreover, the mitogen-activated protein kinases (MAPK) p44/42 (ERK), p38, and p54/46 (JNK) were also activated in a time- and concentration-dependent manner. PD-98059 and SB-239063, specific inhibitors of ERK and p38 MAPK pathways, failed to protect cells against 1 mM SIN-1. However, PD-98059 partially inhibited (60% cell survival) SIN-1 effects at < or =0.25 mM, and this was increased with the inclusion of SB-239063. Therefore, MAPKs may mediate signal transduction pathways induced by peroxynitrite in lung epithelial cells leading to cell death. |
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Authors:
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Elodie Nabeyrat; Gina E Jones; Peter S Fenwick; Peter J Barnes; Louise E Donnelly |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2003-02-21 |
Journal Detail:
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Title: American journal of physiology. Lung cellular and molecular physiology Volume: 284 ISSN: 1040-0605 ISO Abbreviation: Am. J. Physiol. Lung Cell Mol. Physiol. Publication Date: 2003 Jun |
Date Detail:
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Created Date: 2003-05-08 Completed Date: 2003-06-23 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 100901229 Medline TA: Am J Physiol Lung Cell Mol Physiol Country: United States |
Other Details:
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Languages: eng Pagination: L1112-20 Citation Subset: IM |
Affiliation:
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Thoracic Medicine, National Heart and Lung Institute, Faculty of Medicine, Imperial College of Science, Technology and Medicine, London SW3 6LY, United Kingdom. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Bronchi
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cytology*,
enzymology* Cell Death / drug effects*, physiology Cell Line Dose-Response Relationship, Drug Enzyme Inhibitors / pharmacology Epithelial Cells / cytology, enzymology Flavonoids / pharmacology Humans MAP Kinase Signaling System / drug effects, physiology* Molsidomine / analogs & derivatives*, pharmacology Nitric Oxide / metabolism Nitric Oxide Donors / pharmacology Peroxynitrous Acid / pharmacology* Respiratory Mucosa / cytology, enzymology Superoxides / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Enzyme Inhibitors; 0/Flavonoids; 0/Nitric Oxide Donors; 0/PD 98059; 10102-43-9/Nitric Oxide; 11062-77-4/Superoxides; 14691-52-2/Peroxynitrous Acid; 25717-80-0/Molsidomine; 33876-97-0/3-morpholino-sydnonimine |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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