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Article: Interaction of caveolin-1, nitric oxide, and nitric oxide synthases in hypoxic human SK-N-MC neuroblastoma cells

TitleInteraction of caveolin-1, nitric oxide, and nitric oxide synthases in hypoxic human SK-N-MC neuroblastoma cells
Authors
KeywordsCaveolin-1
Hypoxia
Neuroblastoma cells
Nitric oxide
Nitric oxide synthases
Issue Date2008
PublisherBlackwell Publishing Ltd
Citation
Journal Of Neurochemistry, 2008, v. 107 n. 2, p. 478-487 How to Cite?
AbstractNeuroblastoma 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 NG-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. © 2008 The Authors.
Persistent Identifierhttp://hdl.handle.net/10722/59681
ISSN
2015 Impact Factor: 3.842
2015 SCImago Journal Rankings: 2.021
ISI Accession Number ID
Funding AgencyGrant Number
Hong Kong RGC GRF7495/04M
7748/08M
Funding Information:

This work was supported by Hong Kong RGC GRF Grant No. 7495/04M and No. 7748/08M.

References

 

DC FieldValueLanguage
dc.contributor.authorShen, Jen_HK
dc.contributor.authorLee, Wen_HK
dc.contributor.authorLi, Yen_HK
dc.contributor.authorLau, CFen_HK
dc.contributor.authorNg, KMen_HK
dc.contributor.authorFung, MLen_HK
dc.contributor.authorLiu, KJen_HK
dc.date.accessioned2010-05-31T03:55:09Z-
dc.date.available2010-05-31T03:55:09Z-
dc.date.issued2008en_HK
dc.identifier.citationJournal Of Neurochemistry, 2008, v. 107 n. 2, p. 478-487en_HK
dc.identifier.issn0022-3042en_HK
dc.identifier.urihttp://hdl.handle.net/10722/59681-
dc.description.abstractNeuroblastoma 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 NG-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. © 2008 The Authors.en_HK
dc.languageengen_HK
dc.publisherBlackwell Publishing Ltden_HK
dc.relation.ispartofJournal of Neurochemistryen_HK
dc.rightsJournal of Neurochemistry. Copyright © Blackwell Publishing Ltd.en_HK
dc.subjectCaveolin-1en_HK
dc.subjectHypoxiaen_HK
dc.subjectNeuroblastoma cellsen_HK
dc.subjectNitric oxideen_HK
dc.subjectNitric oxide synthasesen_HK
dc.titleInteraction of caveolin-1, nitric oxide, and nitric oxide synthases in hypoxic human SK-N-MC neuroblastoma cellsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-3042&volume=107&spage=478&epage=487&date=2008&atitle=Interaction+of+caveolin-1,+nitric+oxide,+and+nitric+oxide+synthases+in+hypoxic+human+SK-N-MC+neuroblastoma+cells.en_HK
dc.identifier.emailShen, J: shenjg@hku.hken_HK
dc.identifier.emailNg, KM: skykmng@hkucc.hku.hken_HK
dc.identifier.emailFung, ML: fungml@hkucc.hku.hken_HK
dc.identifier.authorityShen, J=rp00487en_HK
dc.identifier.authorityNg, KM=rp01670en_HK
dc.identifier.authorityFung, ML=rp00433en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1471-4159.2008.05630.xen_HK
dc.identifier.pmid18717816-
dc.identifier.scopuseid_2-s2.0-53149114868en_HK
dc.identifier.hkuros154245en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-53149114868&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume107en_HK
dc.identifier.issue2en_HK
dc.identifier.spage478en_HK
dc.identifier.epage487en_HK
dc.identifier.isiWOS:000259949900015-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridShen, J=7404929947en_HK
dc.identifier.scopusauthoridLee, W=12788473400en_HK
dc.identifier.scopusauthoridLi, Y=26643036800en_HK
dc.identifier.scopusauthoridLau, CF=25122803900en_HK
dc.identifier.scopusauthoridNg, KM=25122990200en_HK
dc.identifier.scopusauthoridFung, ML=7101955092en_HK
dc.identifier.scopusauthoridLiu, KJ=7404200456en_HK
dc.identifier.citeulike3374630-

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