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Conference Paper: Brain uncoupling protein-2 mediates neuronal survival by leptin against mitochondrial dysfunction and ATP deficiency

TitleBrain uncoupling protein-2 mediates neuronal survival by leptin against mitochondrial dysfunction and ATP deficiency
Authors
Issue Date2008
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/76507419
Citation
The 12th International Congress of Parkinson's Disease and Movement Disorders, Chicago, IL., 22-28 June 2008. In Movement Disorders, 2008, v. 23 suppl. S1, p. S18, abstract no. 40 How to Cite?
AbstractOBJECTIVE: To determine neuroprotective properties of neuronal uncoupling protein-2 (UCP2) and leptin under MPP1-induced oxidative stress and mitochondrial dysfunction. BACKGROUND: Mitochondrial dysfunction, ATP deficiency, and oxidative stress are associated with Parkinson’s disease (PD). UCPs delink ATP production from oxidative phosphorylation in mitochondria to reduce oxidative stress. UCP2 is expressed in brain. Leptin regulates energy homeostasis and metabolism, and is neuroprotective against apoptosis. We observed induction of UCP2 expression after leptin treatment in neuronal cultures. We hypothesize that leptin may preserve neuronal energy levels by modulating mitochondrial efficiency and ATP production via UCPs. METHODS: Neuroprotective effects of leptin were studied in MPP1-induced mitochondrial dysfunction and oxidative stress in SH-SY5Y cells. UCP2 was stably knocked down by microRNA. Cells were exposed to MPP1 (0.5 mM) with and without leptin (30 lg/ml) for 24 hr. ATP levels were monitored by luciferase assay; level of cell death by cell proliferation assay; mitochondrial membrane potential and oxidative stress by flow cytometry after fluorescent staining of JC-1 and DHE, respectively. RESULTS: Leptin alone increased neuronal ATP supply, and was protective against MPP1-induced cell death, and associated with an increase in UCP2 expression. Leptin also significantly attenuated MPP1-induced ATP deficiency and mitochondrial depolarization. Stable knockdown of UCP2 expression reduced ATP levels, and completely abolished leptin protection against MPP1-induced cell death and ATP deficiency compared with vector controls. CONCLUSIONS: Leptin promotes neuronal survival by restoring MPP1-induced mitochondrial depolarization and ATP deficiency. Knockdown of UCP2 abolished leptin protection. Our results show that UCP2 is inducible and is critical in mediating the neuroprotective effects of leptin.
DescriptionThis journal suppl. entitled: Supplement: Abstracts of The Movement Disorder Society's Twelfth International Congress of Parkinson's Disease and Movement Disorders
Persistent Identifierhttp://hdl.handle.net/10722/101758
ISSN
2015 Impact Factor: 6.01
2015 SCImago Journal Rankings: 2.733

 

DC FieldValueLanguage
dc.contributor.authorHo, WLen_HK
dc.contributor.authorHo, WMen_HK
dc.contributor.authorKwok, HHen_HK
dc.contributor.authorChu, ACYen_HK
dc.contributor.authorLiu, Hen_HK
dc.contributor.authorKung, MHWen_HK
dc.contributor.authorRamsden, DBen_HK
dc.contributor.authorHo, SLen_HK
dc.date.accessioned2010-09-25T20:03:08Z-
dc.date.available2010-09-25T20:03:08Z-
dc.date.issued2008en_HK
dc.identifier.citationThe 12th International Congress of Parkinson's Disease and Movement Disorders, Chicago, IL., 22-28 June 2008. In Movement Disorders, 2008, v. 23 suppl. S1, p. S18, abstract no. 40-
dc.identifier.issn0885-3185-
dc.identifier.urihttp://hdl.handle.net/10722/101758-
dc.descriptionThis journal suppl. entitled: Supplement: Abstracts of The Movement Disorder Society's Twelfth International Congress of Parkinson's Disease and Movement Disorders-
dc.description.abstractOBJECTIVE: To determine neuroprotective properties of neuronal uncoupling protein-2 (UCP2) and leptin under MPP1-induced oxidative stress and mitochondrial dysfunction. BACKGROUND: Mitochondrial dysfunction, ATP deficiency, and oxidative stress are associated with Parkinson’s disease (PD). UCPs delink ATP production from oxidative phosphorylation in mitochondria to reduce oxidative stress. UCP2 is expressed in brain. Leptin regulates energy homeostasis and metabolism, and is neuroprotective against apoptosis. We observed induction of UCP2 expression after leptin treatment in neuronal cultures. We hypothesize that leptin may preserve neuronal energy levels by modulating mitochondrial efficiency and ATP production via UCPs. METHODS: Neuroprotective effects of leptin were studied in MPP1-induced mitochondrial dysfunction and oxidative stress in SH-SY5Y cells. UCP2 was stably knocked down by microRNA. Cells were exposed to MPP1 (0.5 mM) with and without leptin (30 lg/ml) for 24 hr. ATP levels were monitored by luciferase assay; level of cell death by cell proliferation assay; mitochondrial membrane potential and oxidative stress by flow cytometry after fluorescent staining of JC-1 and DHE, respectively. RESULTS: Leptin alone increased neuronal ATP supply, and was protective against MPP1-induced cell death, and associated with an increase in UCP2 expression. Leptin also significantly attenuated MPP1-induced ATP deficiency and mitochondrial depolarization. Stable knockdown of UCP2 expression reduced ATP levels, and completely abolished leptin protection against MPP1-induced cell death and ATP deficiency compared with vector controls. CONCLUSIONS: Leptin promotes neuronal survival by restoring MPP1-induced mitochondrial depolarization and ATP deficiency. Knockdown of UCP2 abolished leptin protection. Our results show that UCP2 is inducible and is critical in mediating the neuroprotective effects of leptin.-
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/76507419-
dc.relation.ispartofMovement Disordersen_HK
dc.rightsMovement Disorders. Copyright © John Wiley & Sons, Inc.-
dc.titleBrain uncoupling protein-2 mediates neuronal survival by leptin against mitochondrial dysfunction and ATP deficiencyen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailHo, WL: hwl2002@hkusua.hku.hken_HK
dc.identifier.emailHo, WM: hello_seeka@yahoo.com.hken_HK
dc.identifier.emailKwok, HH: h0394381@hkusua.hku.hken_HK
dc.identifier.emailChu, ACY: bcccy@hkucc.hku.hken_HK
dc.identifier.emailLiu, H: liuld560327@hotmail.comen_HK
dc.identifier.emailKung, MHW: mhwkung@HKUCC.hku.hken_HK
dc.identifier.emailHo, SL: slho@hku.hken_HK
dc.identifier.authorityChu, ACY=rp00505en_HK
dc.identifier.hkuros142952en_HK
dc.identifier.volume23-
dc.identifier.issuesuppl. S1-
dc.identifier.spageS18, abstract no. 40-
dc.identifier.epageS18, abstract no. 40-
dc.publisher.placeUnited States-

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