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Article: Knockdown of uncoupling protein-5 in neuronal SH-SY5Y cells: Effects on MPP+-induced mitochondrial membrane depolarization, ATP deficiency, and oxidative cytotoxicity

TitleKnockdown of uncoupling protein-5 in neuronal SH-SY5Y cells: Effects on MPP+-induced mitochondrial membrane depolarization, ATP deficiency, and oxidative cytotoxicity
Authors
KeywordsATP
Mitochondrial dysfunction
MPP+
Oxidative stress
Parkinson's disease
Uncoupling protein
Issue Date2006
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, 2006, v. 84 n. 6, p. 1358-1366 How to Cite?
AbstractUncoupling proteins (UCPs) uncouple oxidative phosphorylation from ATP synthesis by dissipating proton gradient across mitochondrial inner membrane. The physiological role of neuronal specific UCP5 is unknown. We explored the effects of reduced UCP5 expression on mitochondrial membrane potential (MMP), oxidative stress, ATP levels, and cell viability, under normal and MPP +-induced cytotoxic conditions, in human catecholaminergic SH-SY5Y cells. UCP5 expression was reduced by 56% by siRNA, compared to scrambled-siRNA controls. UCP5 knockdown induced apoptosis but did not affect basal levels of ATP, oxidative stress and MMP in the cells under normal conditions. However, UCP5 knockdown increased MPP+-induced cytotoxicity by 15% and oxidative stress levels by 40%, and partially restored MPP+-induced mitochondrial depolarization by 57%. UCP2 and UCP4 expression were unaffected by UCP5 knockdown. Exacerbation of cytotoxicity, oxidative stress and modification of MMP with reduced UCP5 expression in the face of MPP+ toxicity suggest that UCP5 might be physiologically important in the pathology of oxidative stress-induced neurodegeneration. © 2006 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/163036
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.authorChu, ACYen_HK
dc.contributor.authorKwok, KHHen_HK
dc.contributor.authorKung, MHWen_HK
dc.contributor.authorRamsden, DBen_HK
dc.contributor.authorHo, SLen_HK
dc.date.accessioned2012-09-05T05:26:50Z-
dc.date.available2012-09-05T05:26:50Z-
dc.date.issued2006en_HK
dc.identifier.citationJournal Of Neuroscience Research, 2006, v. 84 n. 6, p. 1358-1366en_HK
dc.identifier.issn0360-4012en_HK
dc.identifier.urihttp://hdl.handle.net/10722/163036-
dc.description.abstractUncoupling proteins (UCPs) uncouple oxidative phosphorylation from ATP synthesis by dissipating proton gradient across mitochondrial inner membrane. The physiological role of neuronal specific UCP5 is unknown. We explored the effects of reduced UCP5 expression on mitochondrial membrane potential (MMP), oxidative stress, ATP levels, and cell viability, under normal and MPP +-induced cytotoxic conditions, in human catecholaminergic SH-SY5Y cells. UCP5 expression was reduced by 56% by siRNA, compared to scrambled-siRNA controls. UCP5 knockdown induced apoptosis but did not affect basal levels of ATP, oxidative stress and MMP in the cells under normal conditions. However, UCP5 knockdown increased MPP+-induced cytotoxicity by 15% and oxidative stress levels by 40%, and partially restored MPP+-induced mitochondrial depolarization by 57%. UCP2 and UCP4 expression were unaffected by UCP5 knockdown. Exacerbation of cytotoxicity, oxidative stress and modification of MMP with reduced UCP5 expression in the face of MPP+ toxicity suggest that UCP5 might be physiologically important in the pathology of oxidative stress-induced neurodegeneration. © 2006 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.subjectATPen_HK
dc.subjectMitochondrial dysfunctionen_HK
dc.subjectMPP+en_HK
dc.subjectOxidative stressen_HK
dc.subjectParkinson's diseaseen_HK
dc.subjectUncoupling proteinen_HK
dc.subject.mesh1-Methyl-4-Phenylpyridiniumen_US
dc.subject.meshAdenosine Triphosphate - Deficiencyen_US
dc.subject.meshApoptosis - Physiologyen_US
dc.subject.meshCaspase 3 - Metabolismen_US
dc.subject.meshCell Lineen_US
dc.subject.meshCell Survival - Physiologyen_US
dc.subject.meshDown-Regulation - Physiologyen_US
dc.subject.meshHumansen_US
dc.subject.meshL-Lactate Dehydrogenase - Metabolismen_US
dc.subject.meshMembrane Potentials - Physiologyen_US
dc.subject.meshMembrane Transport Proteins - Genetics - Physiologyen_US
dc.subject.meshMitochondrial Membranes - Physiologyen_US
dc.subject.meshNerve Tissue Proteins - Genetics - Physiologyen_US
dc.subject.meshNeurons - Metabolismen_US
dc.subject.meshOxidation-Reductionen_US
dc.subject.meshOxidative Stress - Physiologyen_US
dc.subject.meshRna, Small Interfering - Geneticsen_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_US
dc.subject.meshSuperoxides - Metabolismen_US
dc.subject.meshTransfectionen_US
dc.titleKnockdown of uncoupling protein-5 in neuronal SH-SY5Y cells: Effects on MPP+-induced mitochondrial membrane depolarization, ATP deficiency, and oxidative cytotoxicityen_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.21034en_HK
dc.identifier.pmid16941493-
dc.identifier.scopuseid_2-s2.0-33750490401en_HK
dc.identifier.hkuros129885-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33750490401&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume84en_HK
dc.identifier.issue6en_HK
dc.identifier.spage1358en_HK
dc.identifier.epage1366en_HK
dc.identifier.isiWOS:000242003000021-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridHo, PWL=25027612100en_HK
dc.identifier.scopusauthoridChu, ACY=24343085700en_HK
dc.identifier.scopusauthoridKwok, KHH=7102194193en_HK
dc.identifier.scopusauthoridKung, MHW=36336960300en_HK
dc.identifier.scopusauthoridRamsden, DB=7102612805en_HK
dc.identifier.scopusauthoridHo, SL=25959633500en_HK

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