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Article: Mitochondrial UCP4 attenuates MPP +- and dopamine-induced oxidative stress, mitochondrial depolarization, and ATP deficiency in neurons and is interlinked with UCP2 expression

TitleMitochondrial UCP4 attenuates MPP +- and dopamine-induced oxidative stress, mitochondrial depolarization, and ATP deficiency in neurons and is interlinked with UCP2 expression
Authors
KeywordsATP
Free radicals
Mitochondrial membrane potential
MPP +
Neuroprotection
Oxidative phosphorylation
Oxidative stress
UCP4
Uncoupling proteins
Issue Date2009
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/freeradbiomed
Citation
Free Radical Biology And Medicine, 2009, v. 46 n. 6, p. 810-820 How to Cite?
AbstractMitochondrial uncoupling proteins (UCPs) uncouple oxidative phosphorylation from ATP synthesis. We explored the neuroprotective role of UCP4 with its stable overexpression in SH-SY5Y cells, after exposure to either MPP + or dopamine to induce ATP deficiency and oxidative stress. Cells overexpressing UCP4 proliferated faster in normal cultures and after exposure to MPP + and dopamine. Differentiated UCP4-overexpressing cells survived better when exposed to MPP + with decreased LDH release. Contrary to the mild uncoupling hypothesis, UCP4 overexpression resulted in increased absolute ATP levels (with ADP/ATP ratios similar to those of controls under normal conditions and ADP supplementation) associated with increased respiration rate. Under MPP + toxicity, UCP4 overexpression preserved ATP levels and mitochondrial membrane potential (MMP) and reduced oxidative stress; the preserved ATP level was not due to increased glycolysis. Under MPP + toxicity, the induction of UCP2 expression in vector controls was absent in UCP4-overexpressing cells, suggesting that UCP4 may compensate for UCP2 expression. UCP4 function does not seem to adhere to the mild uncoupling hypothesis in its neuroprotective mechanisms under oxidative stress and ATP deficiency. UCP4 overexpression increases cell survival by inducing oxidative phosphorylation, preserving ATP synthesis and MMP, and reducing oxidative stress. © 2008 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/163228
ISSN
2015 Impact Factor: 5.784
2015 SCImago Journal Rankings: 2.468
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChu, ACYen_US
dc.contributor.authorHo, PWLen_US
dc.contributor.authorKwok, KHHen_US
dc.contributor.authorHo, JWMen_US
dc.contributor.authorChan, KHen_US
dc.contributor.authorLiu, HFen_US
dc.contributor.authorKung, MHWen_US
dc.contributor.authorRamsden, DBen_US
dc.contributor.authorHo, SLen_US
dc.date.accessioned2012-09-05T05:28:58Z-
dc.date.available2012-09-05T05:28:58Z-
dc.date.issued2009en_US
dc.identifier.citationFree Radical Biology And Medicine, 2009, v. 46 n. 6, p. 810-820en_US
dc.identifier.issn0891-5849en_US
dc.identifier.urihttp://hdl.handle.net/10722/163228-
dc.description.abstractMitochondrial uncoupling proteins (UCPs) uncouple oxidative phosphorylation from ATP synthesis. We explored the neuroprotective role of UCP4 with its stable overexpression in SH-SY5Y cells, after exposure to either MPP + or dopamine to induce ATP deficiency and oxidative stress. Cells overexpressing UCP4 proliferated faster in normal cultures and after exposure to MPP + and dopamine. Differentiated UCP4-overexpressing cells survived better when exposed to MPP + with decreased LDH release. Contrary to the mild uncoupling hypothesis, UCP4 overexpression resulted in increased absolute ATP levels (with ADP/ATP ratios similar to those of controls under normal conditions and ADP supplementation) associated with increased respiration rate. Under MPP + toxicity, UCP4 overexpression preserved ATP levels and mitochondrial membrane potential (MMP) and reduced oxidative stress; the preserved ATP level was not due to increased glycolysis. Under MPP + toxicity, the induction of UCP2 expression in vector controls was absent in UCP4-overexpressing cells, suggesting that UCP4 may compensate for UCP2 expression. UCP4 function does not seem to adhere to the mild uncoupling hypothesis in its neuroprotective mechanisms under oxidative stress and ATP deficiency. UCP4 overexpression increases cell survival by inducing oxidative phosphorylation, preserving ATP synthesis and MMP, and reducing oxidative stress. © 2008 Elsevier Inc. All rights reserved.en_US
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/freeradbiomeden_US
dc.relation.ispartofFree Radical Biology and Medicineen_US
dc.rightsFree Radical Biology & Medicine. Copyright © Elsevier Inc.-
dc.subjectATP-
dc.subjectFree radicals-
dc.subjectMitochondrial membrane potential-
dc.subjectMPP +-
dc.subjectNeuroprotection-
dc.subjectOxidative phosphorylation-
dc.subjectOxidative stress-
dc.subjectUCP4-
dc.subjectUncoupling proteins-
dc.subject.mesh1-Methyl-4-Phenylpyridinium - Metabolismen_US
dc.subject.meshAdenosine Triphosphate - Genetics - Metabolismen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAntibodies - Immunologyen_US
dc.subject.meshApoptosisen_US
dc.subject.meshCell Fractionationen_US
dc.subject.meshCell Lineen_US
dc.subject.meshCloning, Molecularen_US
dc.subject.meshDopamine - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunizationen_US
dc.subject.meshImmunodominant Epitopes - Chemistry - Immunologyen_US
dc.subject.meshIon Channels - Genetics - Metabolismen_US
dc.subject.meshMembrane Potential, Mitochondrialen_US
dc.subject.meshMembrane Transport Proteins - Genetics - Immunology - Metabolismen_US
dc.subject.meshMitochondria - Genetics - Immunology - Metabolismen_US
dc.subject.meshMitochondrial Proteins - Genetics - Metabolismen_US
dc.subject.meshNeurons - Immunology - Metabolism - Pathologyen_US
dc.subject.meshOxidative Stressen_US
dc.subject.meshPeptides - Administration & Dosage - Chemical Synthesisen_US
dc.subject.meshRna, Small Interferingen_US
dc.subject.meshSheepen_US
dc.titleMitochondrial UCP4 attenuates MPP +- and dopamine-induced oxidative stress, mitochondrial depolarization, and ATP deficiency in neurons and is interlinked with UCP2 expressionen_US
dc.typeArticleen_US
dc.identifier.emailChu, ACY:bcccy@hkucc.hku.hken_US
dc.identifier.emailHo, PWL:hwl2002@hku.hken_US
dc.identifier.emailHo, SL:slho@hku.hken_US
dc.identifier.authorityChu, ACY=rp00505en_US
dc.identifier.authorityHo, PWL=rp00259en_US
dc.identifier.authorityHo, SL=rp00240en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.freeradbiomed.2008.12.015en_US
dc.identifier.pmid19150400-
dc.identifier.scopuseid_2-s2.0-60449092709en_US
dc.identifier.hkuros154930-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-60449092709&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume46en_US
dc.identifier.issue6en_US
dc.identifier.spage810en_US
dc.identifier.epage820en_US
dc.identifier.eissn1873-4596-
dc.identifier.isiWOS:000264061400013-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridChu, ACY=24343085700en_US
dc.identifier.scopusauthoridHo, PWL=25027612100en_US
dc.identifier.scopusauthoridKwok, KHH=7102194193en_US
dc.identifier.scopusauthoridHo, JWM=8685214100en_US
dc.identifier.scopusauthoridChan, KH=7406034963en_US
dc.identifier.scopusauthoridLiu, HF=27170235100en_US
dc.identifier.scopusauthoridKung, MHW=36336960300en_US
dc.identifier.scopusauthoridRamsden, DB=7102612805en_US
dc.identifier.scopusauthoridHo, SL=25959633500en_US

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