| Reactive nitrogen species block cell cycle re-entry through sustained production of hydrogen peroxide. | |
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MedLine Citation:
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PMID: 12600834 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Endogenous sources of reactive nitrogen species (RNS) act as second messengers in a variety of cell signaling events, whereas environmental sources of RNS like nitrogen dioxide (NO2) inhibit cell survival and growth through covalent modification of cellular macromolecules. To examine the effects of RNS on cell cycle progression, murine type II alveolar C10 cells arrested in G0 by serum deprivation were exposed to either NO2 or SIN-1, a generator of RNS, during cell cycle re-entry. In serum-stimulated cells, RNS did not prevent the immediate early gene response by AP-1, but rather blocked cyclin D1 gene expression, resulting cell cycle arrest at the boundary between G0 and G1. Dichlorofluorescin diacetate (DCF) fluorescence indicated that RNS induced sustained production of intracellular hydrogen peroxide (H2O2), which normally is produced only transiently in response to serum growth factors. Loading cells with catalase did not diminish the formation of 3-nitrotyrosine on the cell surface, but rather prevented enhanced DCF fluorescence and rescued cyclin D1 expression and S phase entry. These studies indicate environmental RNS interfere with cell cycle re-entry through an H2O2-dependent mechanism that influences expression of cyclin D1 and progression from G0 to the G1 phase of the cell cycle. |
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Authors:
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Ziqiang Yuan; Harriet Schellekens; Loraine Warner; Yvonne Janssen-Heininger; Peter Burch; Nicholas H Heintz |
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Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, P.H.S. Date: 2003-01-10 |
Journal Detail:
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Title: American journal of respiratory cell and molecular biology Volume: 28 ISSN: 1044-1549 ISO Abbreviation: Am. J. Respir. Cell Mol. Biol. Publication Date: 2003 Jun |
Date Detail:
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Created Date: 2003-05-22 Completed Date: 2003-07-10 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 8917225 Medline TA: Am J Respir Cell Mol Biol Country: United States |
Other Details:
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Languages: eng Pagination: 705-12 Citation Subset: IM |
Affiliation:
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Department of Pathology, University of Vermont College of Medicine, Burlington VT 05465, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Catalase / metabolism, pharmacology Cell Cycle / drug effects, physiology* Cells, Cultured Cyclin D1 / drug effects, genetics Epithelial Cells / drug effects, metabolism Fluoresceins / analysis, metabolism Gene Expression Regulation / drug effects Hydrogen Peroxide / metabolism*, pharmacology Mice Molsidomine / analogs & derivatives*, pharmacology Nitric Oxide Donors / pharmacology Nitrogen Dioxide / metabolism, pharmacology* Oxidants / metabolism*, pharmacology Pulmonary Alveoli / cytology, metabolism Signal Transduction / drug effects, physiology Superoxide Dismutase / metabolism, pharmacology Transcription Factor AP-1 / drug effects, genetics Tyrosine / analogs & derivatives*, metabolism |
| Grant Support | |
ID/Acronym/Agency:
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ES09673/ES/NIEHS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Fluoresceins; 0/Nitric Oxide Donors; 0/Oxidants; 0/Transcription Factor AP-1; 10102-44-0/Nitrogen Dioxide; 136601-57-5/Cyclin D1; 2044-85-1/diacetyldichlorofluorescein; 25717-80-0/Molsidomine; 33876-97-0/3-morpholino-sydnonimine; 3604-79-3/3-nitrotyrosine; 55520-40-6/Tyrosine; 7722-84-1/Hydrogen Peroxide; EC 1.11.1.6/Catalase; EC 1.15.1.1/Superoxide Dismutase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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