| Protection from reoxygenation injury by inhibition of rac1. | |
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MedLine Citation:
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PMID: 9576744 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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We demonstrate that adenoviral-mediated gene transfer of a dominant negative rac1 gene product (N17rac1) inhibits the intracellular burst of reactive oxygen species (ROS) that occurs after reoxygenation of vascular smooth muscle cells. In contrast, expression of a dominant negative ras gene (N17ras) had no effect. Challenge of control cells and cells expressing N17rac1 with a direct oxidant stress produced an equivalent increase in intracellular ROS levels and subsequent cell death. This suggests that N17rac1 expression appears to block production of harmful oxygen radicals and does not act directly or indirectly to scavenge ROS generated during reoxygenation. Expression of N17rac1 results in protection from hypoxia/reoxygenation-induced cell death in a variety of cell types including vascular smooth muscle cells, fibroblasts, endothelial cells, and ventricular myocytes. These results suggest that reoxygenation injury requires the activation of rac proteins, and that inhibition of rac-dependent pathways may be a useful strategy for the prevention of reperfusion injury in ischemic tissues. |
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Authors:
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K S Kim; K Takeda; R Sethi; J B Pracyk; K Tanaka; Y F Zhou; Z X Yu; V J Ferrans; J T Bruder; I Kovesdi; K Irani; P Goldschmidt-Clermont; T Finkel |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: The Journal of clinical investigation Volume: 101 ISSN: 0021-9738 ISO Abbreviation: J. Clin. Invest. Publication Date: 1998 May |
Date Detail:
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Created Date: 1998-06-08 Completed Date: 1998-06-08 Revised Date: 2009-11-18 |
Medline Journal Info:
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Nlm Unique ID: 7802877 Medline TA: J Clin Invest Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 1821-6 Citation Subset: AIM; IM |
Affiliation:
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Cardiology Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Aerobiosis Anaerobiosis Animals Aorta / cytology Cell Death / drug effects Cells, Cultured Free Radical Scavengers GTP-Binding Proteins / antagonists & inhibitors*, genetics Humans Muscle, Smooth, Vascular / drug effects*, pathology Oxygen / pharmacology* Rats Reactive Oxygen Species / metabolism Recombinant Proteins / antagonists & inhibitors Reperfusion Injury / prevention & control Signal Transduction Umbilical Veins / cytology rac GTP-Binding Proteins ras Proteins / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Free Radical Scavengers; 0/Reactive Oxygen Species; 0/Recombinant Proteins; 7782-44-7/Oxygen; EC 3.6.1.-/GTP-Binding Proteins; EC 3.6.5.2/rac GTP-Binding Proteins; EC 3.6.5.2/ras Proteins |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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