File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Methyl-4-phenylpyridinium ion modulates expression of mitochondrial uncoupling proteins 2, 4, and 5 in catecholaminergic (SK-N-SH) cells

TitleMethyl-4-phenylpyridinium ion modulates expression of mitochondrial uncoupling proteins 2, 4, and 5 in catecholaminergic (SK-N-SH) cells
Authors
KeywordsMitochondria
MPP +
Neuroprotection
Oxidative stress
Uncoupling protein
Issue Date2005
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/34828
Citation
Journal Of Neuroscience Research, 2005, v. 81 n. 2, p. 261-268 How to Cite?
AbstractMethyl-4-phenylpyridinium ion (MPP +), a specific dopaminergic neurotoxin, inhibits mitochondrial complex I activity, generates reactive oxygen species (ROS), reduces ATP production, and induces cell death. We explored changes in expression of uncoupling proteins (UCPs 2, 4, and 5) following MPP +-induced toxicity in SK-N-SH cells over 72 hr at the transcriptional (quantification of mRNA by real-time RT-PCR) and translational (Western analysis) levels. UCP5 mRNA and protein were markedly up-regulated (1 mM MPP + at 72 hr caused a twofold increase, P < 0.01), as was UCP4 mRNA, albeit to a much lesser extent. Surprisingly, UCP2 mRNA levels decreased at 24 hr (P < 0.05) but thereafter significantly increased to greater than control levels at 72 hr (P < 0.05), although UCP2 protein levels were decreased throughout (1 mM MPP + at 72 hr caused a reduction of 50%, P < 0.01). The increase in ROS production may be attenuated by UCP4 and UCP5 up-regulation. The consequence of decreased UCP2 levels is unclear, although this may represent an adaptive response to declines in ATP levels, the subsequent increase in mRNA being a response to further increases in oxidative stress. © 2005 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/162873
ISSN
2015 Impact Factor: 2.689
2015 SCImago Journal Rankings: 1.261
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorHo, PWLen_HK
dc.contributor.authorChan, DYLen_HK
dc.contributor.authorKwok, KHHen_HK
dc.contributor.authorChu, ACYen_HK
dc.contributor.authorHo, JWMen_HK
dc.contributor.authorKung, MHWen_HK
dc.contributor.authorRamsden, DBen_HK
dc.contributor.authorHo, SLen_HK
dc.date.accessioned2012-09-05T05:24:37Z-
dc.date.available2012-09-05T05:24:37Z-
dc.date.issued2005en_HK
dc.identifier.citationJournal Of Neuroscience Research, 2005, v. 81 n. 2, p. 261-268en_HK
dc.identifier.issn0360-4012en_HK
dc.identifier.urihttp://hdl.handle.net/10722/162873-
dc.description.abstractMethyl-4-phenylpyridinium ion (MPP +), a specific dopaminergic neurotoxin, inhibits mitochondrial complex I activity, generates reactive oxygen species (ROS), reduces ATP production, and induces cell death. We explored changes in expression of uncoupling proteins (UCPs 2, 4, and 5) following MPP +-induced toxicity in SK-N-SH cells over 72 hr at the transcriptional (quantification of mRNA by real-time RT-PCR) and translational (Western analysis) levels. UCP5 mRNA and protein were markedly up-regulated (1 mM MPP + at 72 hr caused a twofold increase, P < 0.01), as was UCP4 mRNA, albeit to a much lesser extent. Surprisingly, UCP2 mRNA levels decreased at 24 hr (P < 0.05) but thereafter significantly increased to greater than control levels at 72 hr (P < 0.05), although UCP2 protein levels were decreased throughout (1 mM MPP + at 72 hr caused a reduction of 50%, P < 0.01). The increase in ROS production may be attenuated by UCP4 and UCP5 up-regulation. The consequence of decreased UCP2 levels is unclear, although this may represent an adaptive response to declines in ATP levels, the subsequent increase in mRNA being a response to further increases in oxidative stress. © 2005 Wiley-Liss, Inc.en_HK
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/34828en_HK
dc.relation.ispartofJournal of Neuroscience Researchen_HK
dc.rightsJournal of Neuroscience Research. Copyright © John Wiley & Sons, Inc.-
dc.subjectMitochondriaen_HK
dc.subjectMPP +en_HK
dc.subjectNeuroprotectionen_HK
dc.subjectOxidative stressen_HK
dc.subjectUncoupling proteinen_HK
dc.subject.mesh1-Methyl-4-Phenylpyridinium - Toxicityen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshDopamine - Metabolismen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshGene Expression Regulation - Drug Effectsen_US
dc.subject.meshHumansen_US
dc.subject.meshIon Channelsen_US
dc.subject.meshMembrane Transport Proteins - Drug Effects - Genetics - Metabolismen_US
dc.subject.meshMitochondria - Drug Effects - Metabolismen_US
dc.subject.meshMitochondrial Proteins - Drug Effects - Genetics - Metabolismen_US
dc.subject.meshNerve Tissue Proteins - Drug Effects - Genetics - Metabolismen_US
dc.subject.meshNeurons - Drug Effects - Metabolismen_US
dc.subject.meshNeurotoxins - Toxicityen_US
dc.subject.meshRna, Messenger - Analysisen_US
dc.titleMethyl-4-phenylpyridinium ion modulates expression of mitochondrial uncoupling proteins 2, 4, and 5 in catecholaminergic (SK-N-SH) cellsen_HK
dc.typeArticleen_HK
dc.identifier.emailHo, PWL: hwl2002@hku.hken_HK
dc.identifier.emailChu, ACY: bcccy@hkucc.hku.hken_HK
dc.identifier.emailHo, SL: slho@hku.hken_HK
dc.identifier.authorityHo, PWL=rp00259en_HK
dc.identifier.authorityChu, ACY=rp00505en_HK
dc.identifier.authorityHo, SL=rp00240en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/jnr.20569en_HK
dc.identifier.pmid15948157-
dc.identifier.scopuseid_2-s2.0-23844467747en_HK
dc.identifier.hkuros105584-
dc.identifier.hkuros151954-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-23844467747&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume81en_HK
dc.identifier.issue2en_HK
dc.identifier.spage261en_HK
dc.identifier.epage268en_HK
dc.identifier.isiWOS:000230230700013-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridHo, PWL=25027612100en_HK
dc.identifier.scopusauthoridChan, DYL=26530683900en_HK
dc.identifier.scopusauthoridKwok, KHH=7102194193en_HK
dc.identifier.scopusauthoridChu, ACY=24343085700en_HK
dc.identifier.scopusauthoridHo, JWM=8685214100en_HK
dc.identifier.scopusauthoridKung, MHW=36336960300en_HK
dc.identifier.scopusauthoridRamsden, DB=7102612805en_HK
dc.identifier.scopusauthoridHo, SL=25959633500en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats