| Interaction of caveolin-1, nitric oxide, and nitric oxide synthases in hypoxic human SK-N-MC neuroblastoma cells. | |
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MedLine Citation:
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PMID: 18717816 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Neuroblastoma cells are capable of hypoxic adaptation, but the mechanisms involved are not fully understood. We hypothesized that caveolin-1 (cav-1), a plasma membrane signal molecule, might play a role in protecting neuroblastoma cells from oxidative injury by modulating nitric oxide (NO) production. We investigated the alterations of cav-1, cav-2, nitric oxide synthases (NOS), and NO levels in human SK-N-MC neuroblastoma cells exposed to hypoxia with 2% [O2]. The major discoveries include: (i) cav-1 but not cav-2 was up-regulated in the cells exposed to 15 h of hypoxia; (ii) NO donor 1-[N, N-di-(2-aminoethyl) amino] diazen-1-ium-1, 2-diolate up-regulated the expression of cav-1, whereas the non-selective NOS inhibitor N(G)-nitro-L-arginine methyl ester and inducible NOS (iNOS) inhibitor 1400W each abolished the increase in cav-1 expression in the hypoxic SK-N-MC cells. These results suggest that iNOS-induced NO production contributes to the up-regulation of cav-1 in the hypoxic SK-N-MC cells. Furthermore, we studied the roles played by cav-1 in regulating NO, NOS, and apoptotic cell death in the SK-N-MC cells subjected to 15 h of hypoxic treatment. Both cav-1 transfection and cav-1 scaffolding domain peptide abolished the induction of iNOS, reduced the production of NO, and reduced the rates of apoptotic cell death in the hypoxic SK-N-MC cells. These results suggest that increased expression of cav-1 in response to hypoxic stimulation could prevent oxidative injury induced by reactive oxygen species. The interactions of cav-1, NO, and NOS could be an important signal pathway in protecting the neuroblastoma cells from oxidative injury, contributing to the hypoxic tolerance of neuroblastoma cells. |
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Authors:
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Jiangang Shen; Waisin Lee; Yue Li; Chi Fai Lau; Kwong Man Ng; Man Lung Fung; Ke Jian Liu |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2008-08-20 |
Journal Detail:
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Title: Journal of neurochemistry Volume: 107 ISSN: 1471-4159 ISO Abbreviation: J. Neurochem. Publication Date: 2008 Oct |
Date Detail:
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Created Date: 2008-11-07 Completed Date: 2008-12-24 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 2985190R Medline TA: J Neurochem Country: England |
Other Details:
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Languages: eng Pagination: 478-87 Citation Subset: IM |
Affiliation:
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School of Chinese Medicine, The University of Hong Kong, Hong Kong. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Analysis of Variance Annexin A5 / metabolism Caveolin 1 / genetics, metabolism* Caveolin 2 / genetics, metabolism Cell Hypoxia / drug effects, physiology* Cell Line, Tumor DEET / pharmacology Dose-Response Relationship, Drug Enzyme Inhibitors / pharmacology Gene Expression Regulation / drug effects, physiology Humans NG-Nitroarginine Methyl Ester / pharmacology Neuroblastoma Nitric Oxide / genetics, metabolism*, pharmacology Nitric Oxide Synthase Type II / genetics, metabolism* RNA, Messenger / metabolism Time Factors Transfection / methods |
| Chemical | |
Reg. No./Substance:
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0/Annexin A5; 0/Caveolin 1; 0/Caveolin 2; 0/Enzyme Inhibitors; 0/RNA, Messenger; 10102-43-9/Nitric Oxide; 134-62-3/DEET; 50903-99-6/NG-Nitroarginine Methyl Ester; EC 1.14.13.39/Nitric Oxide Synthase Type II |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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