کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6017837 | 1580179 | 2014 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
PPARγ activation rescues mitochondrial function from inhibition of complex I and loss of PINK1
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کلمات کلیدی
sdhARGSSOD1TMRMΔΨmMPTP1-methyl-4-phenylpyridinium ionPPARγCOX-1PGC1Nrf2NQO11-methyl-4-phenyl-1,2,3,6-tetrahydropyridine - 1-methyl-4-phenyl-1،2،3،6-tetrahydropyridineDiOC6(3) - DiOC6 (3)MPP+ - MPP +mtTFA - MTTFNAD(P)H:quinone oxidoreductase 1 - NAD (P) H: کینون اکسیدوردوکتاز 1ROS - ROSTZDs - TZD هاParkinson's disease - بیماری پارکینسونthiazolidinediones - تیازولیدیدونهاdihydroethidium - دی هیدروتیدیمrosiglitazone - روزیگلیتازونsuperoxide dismutase 1 - سوپر اکسید دیسموتاز 1mitochondrial transcription factor A - عامل رونویسی میتوکندری Anuclear factor (erythroid-derived 2)-like 2 - فاکتور هسته ای (erythroid-derived 2) -like 2tetramethylrhodamine methyl ester - متیل استر تترامتیل رودامینDHE - وMitochondrial membrane potential - پتانسیل غشای میتوکندریperoxisome proliferator-activated receptor gamma coactivator 1 - پراکسیوم پرولاکتین گیرنده گاما فعال کننده 1Propidium iodide - پروتئین یدیدPeroxisome proliferator-activated receptor gamma - گاما گیرنده گیرنده فعال پرولیفیزوم فعالReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
عصب شناسی
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چکیده انگلیسی
Parkinson's disease has long been associated with impaired mitochondrial complex I activity, while several gene defects associated with familial Parkinson's involve defects in mitochondrial function or 'quality control' pathways, causing an imbalance between mitochondrial biogenesis and removal of dysfunctional mitochondria by autophagy. Amongst these are mutations of the gene for PTEN-induced kinase 1 (PINK1) in which mitochondrial function is abnormal. Peroxisome proliferator-activated receptor gamma (PPARγ), a nuclear receptor and ligand-dependent transcription factor, regulates pathways of inflammation, lipid and carbohydrate metabolism, antioxidant defences and mitochondrial biogenesis. We have found that inhibition of complex I in human differentiated SHSY-5Y cells by the complex I inhibitor rotenone irreversibly decrease mitochondrial mass, membrane potential and oxygen consumption, while increasing free radical generation and autophagy. Similar changes are seen in PINK1 knockdown cells, in which potential, oxygen consumption and mitochondrial mass are all decreased. In both models, all these changes were reversed by pre-treatment of the cells with the PPARγ agonist, rosiglitazone, which increased mitochondrial biogenesis, increased oxygen consumption and suppressed free radical generation and autophagy. Thus, rosiglitazone is neuroprotective in two different models of mitochondrial dysfunction associated with Parkinson's disease through a direct impact on mitochondrial function.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Neurology - Volume 253, March 2014, Pages 16-27
Journal: Experimental Neurology - Volume 253, March 2014, Pages 16-27
نویسندگان
Juan Carlos Corona, Senio Campos de Souza, Michael R. Duchen,