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Article: Mitochondrial neuronal uncoupling proteins: a target for potential disease-modification in Parkinson's disease

TitleMitochondrial neuronal uncoupling proteins: a target for potential disease-modification in Parkinson's disease
Authors
KeywordsUncoupling proteins
Mitochondria
Parkinson's disease
ATP
Oxidative stress
Neuroprotection
Issue Date2012
PublisherBioMed Central Ltd. The Journal's web site is located at http://www.translationalneurodegeneration.com/
Citation
Translational Neurodegeneration, 2012, v. 1 n. 3, article no. 3 How to Cite?
AbstractThis review gives a brief insight into the role of mitochondrial dysfunction and oxidative stress in the converging pathogenic processes involved in Parkinson's disease (PD). Mitochondria provide cellular energy in the form of ATP via oxidative phosphorylation, but as an integral part of this process, superoxides and other reactive oxygen species are also produced. Excessive free radical production contributes to oxidative stress. Cells have evolved to handle such stress via various endogenous anti-oxidant proteins. One such family of proteins is the mitochondrial uncoupling proteins (UCPs), which are anion carriers located in the mitochondrial inner membrane. There are five known homologues (UCP1 to 5), of which UCP4 and 5 are predominantly expressed in neural cells. In a series of previous publications, we have shown how these neuronal UCPs respond to 1-methyl-4-phenylpyridinium (MPP+; toxic metabolite of MPTP) and dopamine-induced toxicity to alleviate neuronal cell death by preserving ATP levels and mitochondrial membrane potential, and reducing oxidative stress. We also showed how their expression can be influenced by nuclear factor kappa-B (NF-kappaB) signaling pathway specifically in UCP4. Furthermore, we previously reported an interesting link between PD and metabolic processes through the protective effects of leptin (hormone produced by adipocytes) acting via UCP2 against MPP+-induced toxicity. There is increasing evidence that these endogenous neuronal UCPs can play a vital role to protect neurons against various pathogenic stresses including those associated with PD. Their expression, which can be induced, may well be a potential therapeutic target for various drugs to alleviate the harmful effects of pathogenic processes in PD and hence modify the progression of this disease.
Persistent Identifierhttp://hdl.handle.net/10722/145900
ISSN
2015 SCImago Journal Rankings: 1.447
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorHo, PWLen_US
dc.contributor.authorHo, JWMen_US
dc.contributor.authorLiu, HFen_US
dc.contributor.authorSo, DHFen_US
dc.contributor.authorTse, ZHMen_US
dc.contributor.authorChan, KHen_US
dc.contributor.authorRamsden, DBen_US
dc.contributor.authorHo, SLen_US
dc.date.accessioned2012-03-27T09:01:23Z-
dc.date.available2012-03-27T09:01:23Z-
dc.date.issued2012en_US
dc.identifier.citationTranslational Neurodegeneration, 2012, v. 1 n. 3, article no. 3en_US
dc.identifier.issn2047-9158-
dc.identifier.urihttp://hdl.handle.net/10722/145900-
dc.description.abstractThis review gives a brief insight into the role of mitochondrial dysfunction and oxidative stress in the converging pathogenic processes involved in Parkinson's disease (PD). Mitochondria provide cellular energy in the form of ATP via oxidative phosphorylation, but as an integral part of this process, superoxides and other reactive oxygen species are also produced. Excessive free radical production contributes to oxidative stress. Cells have evolved to handle such stress via various endogenous anti-oxidant proteins. One such family of proteins is the mitochondrial uncoupling proteins (UCPs), which are anion carriers located in the mitochondrial inner membrane. There are five known homologues (UCP1 to 5), of which UCP4 and 5 are predominantly expressed in neural cells. In a series of previous publications, we have shown how these neuronal UCPs respond to 1-methyl-4-phenylpyridinium (MPP+; toxic metabolite of MPTP) and dopamine-induced toxicity to alleviate neuronal cell death by preserving ATP levels and mitochondrial membrane potential, and reducing oxidative stress. We also showed how their expression can be influenced by nuclear factor kappa-B (NF-kappaB) signaling pathway specifically in UCP4. Furthermore, we previously reported an interesting link between PD and metabolic processes through the protective effects of leptin (hormone produced by adipocytes) acting via UCP2 against MPP+-induced toxicity. There is increasing evidence that these endogenous neuronal UCPs can play a vital role to protect neurons against various pathogenic stresses including those associated with PD. Their expression, which can be induced, may well be a potential therapeutic target for various drugs to alleviate the harmful effects of pathogenic processes in PD and hence modify the progression of this disease.-
dc.languageengen_US
dc.publisherBioMed Central Ltd. The Journal's web site is located at http://www.translationalneurodegeneration.com/-
dc.relation.ispartofTranslational Neurodegenerationen_US
dc.rightsTranslational Neurodegeneration. Copyright © BioMed Central Ltd.-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectUncoupling proteins-
dc.subjectMitochondria-
dc.subjectParkinson's disease-
dc.subjectATP-
dc.subjectOxidative stress-
dc.subjectNeuroprotection-
dc.titleMitochondrial neuronal uncoupling proteins: a target for potential disease-modification in Parkinson's diseaseen_US
dc.typeArticleen_US
dc.identifier.emailHo, PWL: hwl2002@hku.hken_US
dc.identifier.emailHo, JWM: seeka@hku.hken_US
dc.identifier.emailLiu, HF: liuhf@hku.hken_US
dc.identifier.emailTse, ZHM: zerotse@hku.hken_US
dc.identifier.emailChan, KH: koonho@hku.hken_US
dc.identifier.emailHo, SL: slho@hku.hken_US
dc.identifier.authorityHo, PWL=rp00259en_US
dc.identifier.authorityChan, KH=rp00537en_US
dc.identifier.authorityHo, SL=rp00240en_US
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1186/2047-9158-1-3-
dc.identifier.pmid23210978-
dc.identifier.pmcidPMC3506996-
dc.identifier.hkuros198929en_US
dc.identifier.volume1en_US
dc.identifier.issue3, article no. 3en_US
dc.publisher.placeUnited Kingdom-
dc.customcontrol.immutablejt 130418-

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