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Mitochondrial neuronal uncoupling proteins:a target for potential disease-modification in Parkinson’s disease Philip

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Translational Neurodegeneration 2012年第1期1卷 11-19页

作者： WL Ho Jessica WM Ho Hui-Fang Liu Danny HF So Zero HM Tse Koon-Ho Chan David B Ramsden Shu-Leong Ho Division of Neurology Department of MedicineUniversity of Hong KongPokfulamHong Kong SARChina School of Medicine and School of Biosciences University of BirminghamBirminghamUK Research Centre of Heart BrainHormone and Healthy Aging(HBHA)University of Hong KongPokfulamHong Kong SARChina

This 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 *** free radical production contributes to oxidative *** have evolved to handle such stress via various endogenous anti-oxidant *** such family of proteins is the mitochondrial uncoupling proteins(UCPs),which are anion carriers located in the mitochondrial inner *** are five known homologues(UCP1 to 5),of which UCP4 and 5 are predominantly expressed in neural *** 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 *** also showed how their expression can be influenced by nuclear factor kappa-B(NF-B)signaling pathway specifically in ***,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 *** is increasing evidence that these endogenous neuronal UCPs can play a vital role to protect neurons against various pathogenic stresses including those associated with *** 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.

关键词： uncoupling proteins mitochondria Parkinson??s disease ATP oxidative stress neuroprotection

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Reduced cardiac output is associated with decreased mitochondrial efficiency in the non-ischemic ventricular wall of the acute myocardial-infarcted dog

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Cell Research 2006年第3期16卷 297-305页

作者： Zakaria A Almsherqi Malgorzata B Slocinska Yuru Deng Department of Physiology,National University of Singapore,Block MD9,2 Medical Drive,Singapore 117597,Singapore Craig S McLachlan Peter Mossop Department of Medical Imaging,St Vincents Hospital,Melbourne,Fitzroy VIC 3065,Australia Francis E Sluse Rachel Navet Laboratory of Bioenergetics,Institute of Chemistry B6,University of Liége,Start Tilman,B-4000 Liége,Belgium Nikolai Kocherginsky Iouri Kostetski Biophysics Laboratory,Division of Bioengineering,National University of Singapore,Singapore 117576,Singapore Dong-Yun Shi Shan-Lin Liu Department of Biochemistry,Shanghai Medical College of Fudan University,Free Radical Regulation Research Center of Fudan University,Shanghai 200032,China Department of Physiology National University of Singapore Singapore Singapore Department of Medical Imaging St Vincents Hospital Melbourne Australia Laboratory of Bioenergetics Institute of Chemistry B6 University of Liége Start Tilman Liége Belgium Division of Bioengineering Biophysics Laboratory National University of Singapore Singapore Singapore Department of Biochemistry Shanghai Medical College of Fudan University Free Radical Regulation Research Center of Fudan University Shanghai China

Cardiogenic shock is the leading cause of death among patients hospitalized with acute myocardial infarction (MI).Understanding the mechanisms for acute pump failure is therefore *** aim of this study is to examine in anacute MI dog model whether mitochondrial bio-energetic function within non-ischemic wall regions are associated withpump *** MI was produced in dogs via ligation of left anterior descending (LAD) coronary artery,thatresulted in an infract size of about 30% of the left ventricular *** of hemodynamic status,mitochondrialfunction,free radical production and mitochondrial uncoupling protein 3 (UCP3) expression were determined over 24h *** measurements revealed a>50% reduction in cardiac output at 24 h post infarction when com-pared to *** samples were obtained from the posterior non-ischemic wall during acute ***/Oratios for isolated mitochondria from non-ischemic myocardium at 6 h and 24 h were decreased when compared to theADP/O ratios within the same samples with and without palmitic acid (PA).GTP inhibition of (PA)-stimulated state 4respiration in isolated mitochondria from the non-ischemic wall increased by 7% and 33% at 6 h and 24 h post-infarctionrespectively when compared to sham and pre-infarction *** would suggest that the mitochondria are uncoupledand this is supported by an associated increase in UCP3 expression observed on western blots from these same *** samples from the coronary sinus measured by electron paramagnetic resonance (EPR) methods showedan increase in reactive oxygen species (ROS) over baseline at 6 h and 24 h *** conclusion,mitochondrialbio-energetic ADP/O ratios as a result of acute infarction are abnormal within the non-ischemic *** ap-pear to be energetically uncoupled and this is associated with declining pump *** radical production may beassociated with the induction of uncoupling prot

关键词： mitochondria uncoupling proteins bioenergetics infarction cardiogenic shock non-ischemic ventricle

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Mitochondrial determinants of chemoresistance

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Cancer Drug Resistance 2019年第3期2卷 634-646页

作者： Ansooya Bokil Patricia Sancho IIS Aragon Hospital Universitario Miguel ServetZaragoza 50009Spain

Chemoresistance constitute nowadays the major contributor to therapy failure in most *** are main factors that mitigate cell response to therapy,such as target organ,inherent sensitivity to the administered compound,its metabolism,drug efflux and influx or alterations on specific cellular targets,among *** now know that intrinsic properties of cancer cells,including metabolic features,substantially contribute to *** fact,during the last years,numerous reports indicate that cancer cells resistant to chemotherapy demonstrate significant alterations in mitochondrial metabolism,membrane polarization and *** activity and expression of several mitochondrial proteins are modulated under treatment to cope with stress,making these organelles central players in the development of resistance to ***,we review the role of mitochondria in chemoresistant cells in terms of metabolic rewiring and function of key mitochondria-related proteins.

关键词： Mitochondria chemoresistance oxidative phosphorylation fatty acid oxidation metabolism uncoupling proteins ABC transporters

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Sequences and polymorphisms of exons 3 and 4 in porcine UCP2 gene

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Progress in Natural Science:Materials International 2002年第7期 73-74页

作者： FANG Meiying, LIU Chousheng, ZHAO Xingbo, LI Ning and WU Changxin(1. College of Animal Science and Technology, China Agricultural University, Beijing 100094, China 2. National Laboratory for A-gribiotechnology, China Agricultural University, Beijing 100094, China 3. Gansu Institute of Animal and Veterinary Science, Pingliang 744000, China)

uncoupling proteins are mitochondrial membrane transporters, which regulate metabolic pathways of energy balance, and are associated with biological traits of animal body weight, resting metabolic rates and energy conversion. In this study, a region of the exons 3 and 4 of pig UCP2 gene was cloned and analyzed, and a new single nucleotide polymorphic site was detected by PCR-SSCP in five pig breeds. This newfound polymorphism results from a T to G stbstitution at the position of nucleotide 272, which is located in intron3.

关键词： pig uncoupling proteins PCR-SSCP.

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