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Conference Paper: Leptin enhances MPP+-induced mitochondrial dysfunction: a potential for neuroprotection in parkinsonism

TitleLeptin enhances MPP+-induced mitochondrial dysfunction: a potential for neuroprotection in parkinsonism
Authors
Issue Date2006
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/76507419
Citation
The 10th International Congress of Parkinson's disease and Movement Disorders, Kyoto, Japan, 28 October-2 November 2006. In Movement Disorders, 2006, v. 21 suppl 15, p. S346, abstract no. P62 How to Cite?
AbstractOBJECTIVE: To investigate the effects of leptin in MPP+-induced mitochondrial dysfunction and oxidative stress in SH-SY5Y cells. BACKGROUND: Mitochondrial dysfunction, ATP deficiency, and oxidative stress are associated with neuronal cell death in Parkinson’s disease. Studies in regulation of energy balance in neurocircuitry are rapidly emerging. Recent studies have shown that the fat-derived hormone leptin acts as an afferent signal in a negative feedback loop to regulate energy homeostasis through receptor-mediated pathways in the central nervous system. We hypothesize that leptin administration might improve neuronal energy level by modulation of mitochondrial membrane potential and ATP production. METHODS: Leptin (0.1_M) were incubated in SH-SY5Y cells in normal and MPP_-induced (0.5mM) toxicity conditions for 24hr. ATP level, mitochondrial membrane potential and oxidative stress were measured by luciferase-luciferin bioassay and flow cytometry, respectively. RESULTS: MPP+ (0.5mM) at 24hr induced mitochondrial membrane depolarization by 45% and oxidative stress by 2.8 folds in SH-SY5Y cells. Leptin (0.1_M) slightly hyperpolarized mitochondrial membrane potential by 20% and significantly prevented MPP+ induced mitochondrial membrane depolarization. Single regimen of leptin alone remarkably increased ATP level by 48% at 4hr but declined to basal level after 48hr. Leptin had no effect on MPP_ induced oxidative stress. CONCLUSIONS: Leptin treatment improved mitochondrial efficiency by restoration of MPP_-induced mitochondrial depolarization and increase ATP production. These findings might contribute to the understanding of role of leptin in the neurocircuitry and provide insights on therapeutic possibilities in Parkinson’s disease.
DescriptionPoster Session 1
This journal suppl. entitled: Supplement: Tenth International Congress of Parkinson's Disease and Movement Disorders
Persistent Identifierhttp://hdl.handle.net/10722/101339
ISSN
2015 Impact Factor: 6.01
2015 SCImago Journal Rankings: 2.733

 

DC FieldValueLanguage
dc.contributor.authorChu, ACYen_HK
dc.contributor.authorHo, WLen_HK
dc.contributor.authorKwok, HHen_HK
dc.contributor.authorKung, MHWen_HK
dc.contributor.authorRamsden, DBen_HK
dc.contributor.authorHo, SLen_HK
dc.date.accessioned2010-09-25T19:45:38Z-
dc.date.available2010-09-25T19:45:38Z-
dc.date.issued2006en_HK
dc.identifier.citationThe 10th International Congress of Parkinson's disease and Movement Disorders, Kyoto, Japan, 28 October-2 November 2006. In Movement Disorders, 2006, v. 21 suppl 15, p. S346, abstract no. P62en_HK
dc.identifier.issn0885-3185-
dc.identifier.urihttp://hdl.handle.net/10722/101339-
dc.descriptionPoster Session 1-
dc.descriptionThis journal suppl. entitled: Supplement: Tenth International Congress of Parkinson's Disease and Movement Disorders-
dc.description.abstractOBJECTIVE: To investigate the effects of leptin in MPP+-induced mitochondrial dysfunction and oxidative stress in SH-SY5Y cells. BACKGROUND: Mitochondrial dysfunction, ATP deficiency, and oxidative stress are associated with neuronal cell death in Parkinson’s disease. Studies in regulation of energy balance in neurocircuitry are rapidly emerging. Recent studies have shown that the fat-derived hormone leptin acts as an afferent signal in a negative feedback loop to regulate energy homeostasis through receptor-mediated pathways in the central nervous system. We hypothesize that leptin administration might improve neuronal energy level by modulation of mitochondrial membrane potential and ATP production. METHODS: Leptin (0.1_M) were incubated in SH-SY5Y cells in normal and MPP_-induced (0.5mM) toxicity conditions for 24hr. ATP level, mitochondrial membrane potential and oxidative stress were measured by luciferase-luciferin bioassay and flow cytometry, respectively. RESULTS: MPP+ (0.5mM) at 24hr induced mitochondrial membrane depolarization by 45% and oxidative stress by 2.8 folds in SH-SY5Y cells. Leptin (0.1_M) slightly hyperpolarized mitochondrial membrane potential by 20% and significantly prevented MPP+ induced mitochondrial membrane depolarization. Single regimen of leptin alone remarkably increased ATP level by 48% at 4hr but declined to basal level after 48hr. Leptin had no effect on MPP_ induced oxidative stress. CONCLUSIONS: Leptin treatment improved mitochondrial efficiency by restoration of MPP_-induced mitochondrial depolarization and increase ATP production. These findings might contribute to the understanding of role of leptin in the neurocircuitry and provide insights on therapeutic possibilities in Parkinson’s disease.-
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.titleLeptin enhances MPP+-induced mitochondrial dysfunction: a potential for neuroprotection in parkinsonismen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailChu, ACY: bcccy@hkucc.hku.hken_HK
dc.identifier.emailHo, WL: hwl2002@hkusua.hku.hken_HK
dc.identifier.emailKwok, HH: h0394381@hkusua.hku.hken_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.doi10.1002/mds.21246-
dc.identifier.hkuros129896en_HK
dc.identifier.volume21en_HK
dc.identifier.issuesuppl. 15en_HK
dc.identifier.spageS346, abstract no. P62en_HK
dc.identifier.epageS346, abstract no. P62-
dc.publisher.placeUnited States-

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