File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
  • Find via Find It@HKUL
Supplementary

Conference Paper: Uncoupling protein-4 (UCP4) increases neuronal ATP production via respiratory Complex-II activation - a bioenergetic study

TitleUncoupling protein-4 (UCP4) increases neuronal ATP production via respiratory Complex-II activation - a bioenergetic study
Authors
Issue Date2011
PublisherElsevier Ltd. The Journal's web site is located at http://www.elsevier.com/locate/parkreldis
Citation
The 19th WFN World Congress on Parkinson's Disease and Related Disorders, Shanghai, China, 11–14 December 2011. In Parkinsonism & Related Disorders, 2012, v. 18 suppl. 2, p. S217, abstract 3.256 How to Cite?
AbstractMitochondrial uncoupling protein-4 (UCP4) can protect neurons against 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP)-induced toxicity but how UCP4 can affect mitochondrial function is unclear. We investigated how UCP4 overexpression can affect mitochondrial bioenergetics in SH-SY5Y neuronal cells. UCP4 overexpression did not alter mitochondrial mass and morphology insitu. UCP4-overexpressing cells had higher oxygen consumption (10.1±0.36%, p < 0.01) under normal culture conditions with 20% greater mitochondrial proton leak than controls (p < 0.01). Increased cellular energy supply was reflected by higher total ATP levels in UCP4-overexpressing cells than controls (p < 0.05). Although classical State-4/State-3 mitochondrial respiration rates were similar between UCP4-overexpressing and control cells, mitochondrial Complex-II REDOX activity in UCP4-overexpressing cells was 30% higher (p < 0.05), but not for Complex-I and -IV. Increased Complex-II activity was associated with 20% higher ADP/O ratio (p < 0.05), but unchanged for Complex-I. These indicate that increased ATP in UCP4-overexpressing cells was produced via Complex-II. ADP/ATP exchange rate reflecting mitochondrial ATP export was not affected by UCP4 overexpression as shown by similar ADP uptake via adenine nucleotide translocase (ANT) with controls. Our findings demonstrate how UCP4 overexpression could increase the efficiency of oxidative phosphorylation and ATP synthesis via Complex-II, suggesting how UCP4 can protect neurons against MPTP-induced ATP deficiency and cell death where Complex-I is inhibited.
DescriptionThis journal suppl. contatin Abstracts of WFN XIX World Congress on Parkinson's Disease and Related Disorders
Persistent Identifierhttp://hdl.handle.net/10722/182114
ISSN
2015 Impact Factor: 3.794
2015 SCImago Journal Rankings: 1.488

 

DC FieldValueLanguage
dc.contributor.authorHo, PWLen_US
dc.contributor.authorHo, JWMen_US
dc.contributor.authorTse, HMen_US
dc.contributor.authorSo, DHFen_US
dc.contributor.authorLiu, HFen_US
dc.contributor.authorChan, KHen_US
dc.contributor.authorKung, MHWen_US
dc.contributor.authorRamsden, DBen_US
dc.contributor.authorHo, SL-
dc.date.accessioned2013-04-17T07:22:02Z-
dc.date.available2013-04-17T07:22:02Z-
dc.date.issued2011en_US
dc.identifier.citationThe 19th WFN World Congress on Parkinson's Disease and Related Disorders, Shanghai, China, 11–14 December 2011. In Parkinsonism & Related Disorders, 2012, v. 18 suppl. 2, p. S217, abstract 3.256en_US
dc.identifier.issn1353-8020-
dc.identifier.urihttp://hdl.handle.net/10722/182114-
dc.descriptionThis journal suppl. contatin Abstracts of WFN XIX World Congress on Parkinson's Disease and Related Disorders-
dc.description.abstractMitochondrial uncoupling protein-4 (UCP4) can protect neurons against 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP)-induced toxicity but how UCP4 can affect mitochondrial function is unclear. We investigated how UCP4 overexpression can affect mitochondrial bioenergetics in SH-SY5Y neuronal cells. UCP4 overexpression did not alter mitochondrial mass and morphology insitu. UCP4-overexpressing cells had higher oxygen consumption (10.1±0.36%, p < 0.01) under normal culture conditions with 20% greater mitochondrial proton leak than controls (p < 0.01). Increased cellular energy supply was reflected by higher total ATP levels in UCP4-overexpressing cells than controls (p < 0.05). Although classical State-4/State-3 mitochondrial respiration rates were similar between UCP4-overexpressing and control cells, mitochondrial Complex-II REDOX activity in UCP4-overexpressing cells was 30% higher (p < 0.05), but not for Complex-I and -IV. Increased Complex-II activity was associated with 20% higher ADP/O ratio (p < 0.05), but unchanged for Complex-I. These indicate that increased ATP in UCP4-overexpressing cells was produced via Complex-II. ADP/ATP exchange rate reflecting mitochondrial ATP export was not affected by UCP4 overexpression as shown by similar ADP uptake via adenine nucleotide translocase (ANT) with controls. Our findings demonstrate how UCP4 overexpression could increase the efficiency of oxidative phosphorylation and ATP synthesis via Complex-II, suggesting how UCP4 can protect neurons against MPTP-induced ATP deficiency and cell death where Complex-I is inhibited.-
dc.languageengen_US
dc.publisherElsevier Ltd. The Journal's web site is located at http://www.elsevier.com/locate/parkreldis-
dc.relation.ispartofParkinsonism & Related Disordersen_US
dc.titleUncoupling protein-4 (UCP4) increases neuronal ATP production via respiratory Complex-II activation - a bioenergetic studyen_US
dc.typeConference_Paperen_US
dc.identifier.emailHo, PWL: hwl2002@hku.hken_US
dc.identifier.emailHo, JWM: seeka@hku.hken_US
dc.identifier.emailTse, HM: zerotse@hku.hken_US
dc.identifier.emailLiu, HF: liuhf@hku.hken_US
dc.identifier.emailKung, MHW: mhwkung@hkucc.hku.hken_US
dc.identifier.emailHo, SL: slho@hku.hken_US
dc.identifier.authorityHo, PWL=rp00259en_US
dc.identifier.authorityHo, SL=rp00240en_US
dc.identifier.hkuros213956en_US
dc.identifier.volume18-
dc.identifier.issuesuppl. 2-
dc.identifier.spageS217, abstract 3.256-
dc.identifier.epageS217, abstract 3.256-
dc.publisher.placeUnited Kingdom-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats