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https://www.readbyqxmd.com/read/28445716/trumping-neurodegeneration-targeting-common-pathways-regulated-by-autosomal-recessive-parkinson-s-disease-genes
#1
REVIEW
Laura Scott, Valina L Dawson, Ted M Dawson
Parkinson's disease (PD) is a neurodegenerative movement disorder characterized by the progressive loss of dopaminergic (DA) neurons. Most PD cases are sporadic; however, rare familial forms have been identified. Autosomal recessive PD (ARPD) results from mutations in Parkin, PINK1, DJ-1, and ATP13A2, while rare, atypical juvenile ARPD result from mutations in FBXO7, DNAJC6, SYNJ1, and PLA2G6. Studying these genes and their function has revealed mitochondrial quality control, protein degradation processes, and oxidative stress responses as common pathways underlying PD pathogenesis...
April 23, 2017: Experimental Neurology
https://www.readbyqxmd.com/read/28438607/obesity-exposed-oocytes-accumulate-and-transmit-damaged-mitochondria-due-to-an-inability-to-activate-mitophagy
#2
Anna L Boudoures, Jessica Saben, Andrea Drury, Suzanne Scheaffer, Zeel Modi, Wendy Zhang, Kelle H Moley
Mitochondria are the most prominent organelle in the oocyte. Somatic cells maintain a healthy population of mitochondria by degrading damaged mitochondria via mitophagy, a specialized autophagy pathway. However, evidence from previous work investigating the more general macroautophagy pathway in oocytes suggests that mitophagy may not be active in the oocyte. This would leave the vast numbers of mitochondria - poised to be inherited by the offspring - vulnerable to damage. Here we test the hypothesis that inactive mitophagy in the oocyte underlies maternal transmission of dysfunctional mitochondria...
April 21, 2017: Developmental Biology
https://www.readbyqxmd.com/read/28438176/the-pink1-p-i368n-mutation-affects-protein-stability-and-ubiquitin-kinase-activity
#3
Maya Ando, Fabienne C Fiesel, Roman Hudec, Thomas R Caulfield, Kotaro Ogaki, Paulina Górka-Skoczylas, Dariusz Koziorowski, Andrzej Friedman, Li Chen, Valina L Dawson, Ted M Dawson, Guojun Bu, Owen A Ross, Zbigniew K Wszolek, Wolfdieter Springer
BACKGROUND: Mutations in PINK1 and PARKIN are the most common causes of recessive early-onset Parkinson's disease (EOPD). Together, the mitochondrial ubiquitin (Ub) kinase PINK1 and the cytosolic E3 Ub ligase PARKIN direct a complex regulated, sequential mitochondrial quality control. Thereby, damaged mitochondria are identified and targeted to degradation in order to prevent their accumulation and eventually cell death. Homozygous or compound heterozygous loss of either gene function disrupts this protective pathway, though at different steps and by distinct mechanisms...
April 24, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/28437683/pink1-and-parkin-emerging-themes-in-mitochondrial-homeostasis
#4
REVIEW
Thomas G McWilliams, Miratul Mk Muqit
The Parkinson's disease (PD)-associated protein kinase, PTEN-induced putative kinase1 (PINK1), and ubiquitin E3 ligase, Parkin function in a common signalling pathway known to regulate mitochondrial network homeostasis and quality control, including mitophagy. The multistep activation of this pathway, as well as an unexpected convergence between the post-translational modifications of ubiquitylation and phosphorylation, has added breadth to our understanding of cellular damage responses during human disease...
April 21, 2017: Current Opinion in Cell Biology
https://www.readbyqxmd.com/read/28435104/drosophila-pink1-and-parkin-loss-of-function-mutants-display-a-range-of-non-motor-parkinson-s-disease-phenotypes
#5
Hannah Julienne, Edgar Buhl, David S Leslie, James J L Hodge
Parkinson's disease (PD) is more commonly associated with its motor symptoms and the related degeneration of dopamine (DA) neurons. However, it is becoming increasingly clear that PD patients also display a wide range of non-motor symptoms, including memory deficits and disruptions of their sleep-wake cycles. These have a large impact on their quality of life, and often precede the onset of motor symptoms, but their etiology is poorly understood. The fruit fly Drosophila has already been successfully used to model PD, and has been used extensively to study relevant non-motor behaviours in other contexts, but little attention has yet been paid to modelling non-motor symptoms of PD in this genetically tractable organism...
April 20, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28434973/long-term-oral-kinetin-does-not-protect-against-%C3%AE-synuclein-induced-neurodegeneration-in-rodent-models-of-parkinson-s-disease
#6
Adam L Orr, Florentine U Rutaganira, Daniel de Roulet, Eric J Huang, Nicholas T Hertz, Kevan M Shokat, Ken Nakamura
Mutations in the mitochondrial kinase PTEN-induced putative kinase 1 (PINK1) cause Parkinson's disease (PD), likely by disrupting PINK1's kinase activity. Although the mechanism(s) underlying how this loss of activity causes degeneration remains unclear, increasing PINK1 activity may therapeutically benefit some forms of PD. However, we must first learn whether restoring PINK1 function prevents degeneration in patients harboring PINK1 mutations, or whether boosting PINK1 function can offer protection in more common causes of PD...
April 20, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28433685/p62-mediated-mitochondrial-clustering-attenuates-apoptosis-induced-by-mitochondrial-depolarization
#7
Bin Xiao, Xiao Deng, Grace G Y Lim, Wei Zhou, Wuan-Ting Saw, Zhi Dong Zhou, Kah-Leong Lim, Eng-King Tan
Parkin/PINK1-mediated mitophagy is implicated in the pathogenesis of Parkinson's disease (PD). Prior to elimination of damaged mitochondria, Parkin translocates to mitochondria and induces mitochondrial clustering. While the mechanism of PINK1-dependent Parkin redistribution to mitochondria is now becoming clear, the role of mitochondrial clustering has been less well understood. In our study, we found that loss of p62 disrupted mitochondrial aggregation and specifically sensitized Parkin-expressing cells to apoptosis induced by mitochondrial depolarization...
April 19, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28431223/pink1-based-screen-shines-light-on-autophagy-enhancers-for-parkinson-s-disease
#8
Dominik Haddad, Ken Nakamura
In this issue of Cell Chemical Biology, Zhang et al. (2017) report a zebrafish model of Parkinson's disease (PD), incorporating the PD-protein PINK1 and rotenone, a toxin linked to PD. Using it as a drug-screening platform, they identify trifluoperazine and other piperazine phenothiazines as protective compounds that enhance autophagy independent of PINK1.
April 20, 2017: Cell Chemical Biology
https://www.readbyqxmd.com/read/28430647/pink1-and-ataxin-2-as-modifiers-of-growth
#9
EDITORIAL
Nesli E Sen, Suzana Gispert, Georg Auburger
No abstract text is available yet for this article.
April 13, 2017: Oncotarget
https://www.readbyqxmd.com/read/28428777/lactobacillus-fermentum-postbiotic-induced-autophagy-as-potential-approach-for-treatment-of-acetaminophen-hepatotoxicity
#10
Miroslav Dinić, Jovanka Lukić, Jelena Djokić, Marina Milenković, Ivana Strahinić, Nataša Golić, Jelena Begović
The aim of this study was to investigate the potential of postbiotics originated from Lactobacillus fermentum BGHV110 strain (HV110) to counteract acetaminophen (APAP)-induced hepatotoxicity in HepG2 cells. This strain was selected according to its autophagy inducing potential, based on previous studies reporting protective role of autophagy in APAP caused cellular damage. Cell viability was assessed using MTT and LDH assays, while autophagy was monitored by qPCR analysis of BECN1, Atg5, p62/SQSTM1, and PINK1 mRNA expression and by Western blot analysis of p62/SQSTM1 and lipidated LC3 accumulation...
2017: Frontiers in Microbiology
https://www.readbyqxmd.com/read/28408429/ubiquitin-and-parkinson-s-disease-through-the-looking-glass-of-genetics
#11
REVIEW
Helen Walden, Miratul M K Muqit
Biochemical alterations found in the brains of Parkinson's disease (PD) patients indicate that cellular stress is a major driver of dopaminergic neuronal loss. Oxidative stress, mitochondrial dysfunction, and ER stress lead to impairment of the homeostatic regulation of protein quality control pathways with a consequent increase in protein misfolding and aggregation and failure of the protein degradation machinery. Ubiquitin signalling plays a central role in protein quality control; however, prior to genetic advances, the detailed mechanisms of how impairment in the ubiquitin system was linked to PD remained mysterious...
April 13, 2017: Biochemical Journal
https://www.readbyqxmd.com/read/28408307/mitochondrial-respiratory-chain-disorganization-in-parkinson-s-disease-relevant-pink1-and-dj1-mutants
#12
Irene Lopez-Fabuel, Lucia Martin-Martin, Monica Resch-Beusher, Garikoitz Azkona, Rosario Sanchez-Pernaute, Juan P Bolaños
Brain mitochondrial complex I (CI) damage is associated with the loss of the dopaminergic neurons of the Substantia Nigra in Parkinson's Disease (PD) patients. However, whether CI inhibition is associated with any alteration of the mitochondrial respiratory chain (MRC) organization in PD patients is unknown. To address this issue, here we analyzed the MRC by blue native gel electrophoresis (BNGE) followed by western blotting, in mitochondria purified from fibroblasts of patients harboring PD-relevant Pink1 mutations...
April 10, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28407488/the-matrix-protein-of-human-parainfluenza-virus-type-3-induces-mitophagy-that-suppresses-interferon-responses
#13
Binbin Ding, Linliang Zhang, Zhifei Li, Yi Zhong, Qiaopeng Tang, Yali Qin, Mingzhou Chen
Mitophagy is a form of autophagy that selectively removes damaged mitochondria. Impaired mitochondria can be tagged by the kinase PINK1, which triggers recruitment of the E3-ubiquitin ligase Parkin and subsequent mitochondrial sequestration within autophagosomes. We previously found that human parainfluenza virus type 3 (HPIV3) infection induces autophagy, but the type and mechanisms of autophagy induction remain unknown. Here, we show that matrix protein (M) of HPIV3 translocates to mitochondria and interacts with Tu translation elongation factor mitochondrial (TUFM)...
April 12, 2017: Cell Host & Microbe
https://www.readbyqxmd.com/read/28399880/quantitative-proteomic-analysis-of-parkin-substrates-in-drosophila-neurons
#14
Aitor Martinez, Benoit Lectez, Juanma Ramirez, Oliver Popp, James D Sutherland, Sylvie Urbé, Gunnar Dittmar, Michael J Clague, Ugo Mayor
BACKGROUND: Parkin (PARK2) is an E3 ubiquitin ligase that is commonly mutated in Familial Parkinson's Disease (PD). In cell culture models, Parkin is recruited to acutely depolarised mitochondria by PINK1. PINK1 activates Parkin activity leading to ubiquitination of multiple proteins, which in turn promotes clearance of mitochondria by mitophagy. Many substrates have been identified using cell culture models in combination with depolarising drugs or proteasome inhibitors, but not in more physiological settings...
April 11, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/28398674/melatonin-protects-cardiac-microvasculature-against-ischemia-reperfusion-injury-via-suppression-of-mitochondrial-fission-vdac1-hk2-mptp-mitophagy-axis
#15
Hao Zhou, Ying Zhang, Shunying Hu, Chen Shi, Pingjun Zhu, Qiang Ma, Qinhua Jin, Feng Cao, Feng Tian, Yundai Chen
The cardiac microvascular system, which is primarily composed of monolayer endothelial cells, is the site of blood supply and nutrient exchange to cardiomyocytes. However, microvascular ischemia/reperfusion injury (IRI) following percutaneous coronary intervention is a woefully neglected topic and few strategies are available to reverse such pathologies. Here, we studied the effects of melatonin on microcirculation IRI and elucidated the underlying mechanism. Melatonin markedly reduced infarcted area, improved cardiac function, restored blood flow and lower microcirculation perfusion defects...
April 11, 2017: Journal of Pineal Research
https://www.readbyqxmd.com/read/28390981/neurochemical-effects-of-the-r-form-of-%C3%AE-lipoic-acid-and-its-neuroprotective-mechanism-in-cellular-models-of-parkinson-s-disease
#16
Hong Zhao, Xingcheng Zhao, Lijuan Liu, Hongxu Zhang, Mingwen Xuan, Zhaohui Guo, Hongcai Wang, Chang Liu
OBJECTIVE: Parkinson's disease (PD) is a common neurodegenerative disease. This study aimed to investigate the effects of the R form of α-lipoic acid (RLA) in cellular models of PD induced by 6-hydroxydopamine (6-OHDA) or 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). METHODS: Cell viability and apoptosis were detected using CCK8 and Annexin V-FITC assays, respectively. Intracellular reactive oxygen species (ROS) were detected by fluorescence staining. ELISA assays were performed to detect the levels of dopamine and α-synuclein...
April 6, 2017: International Journal of Biochemistry & Cell Biology
https://www.readbyqxmd.com/read/28379295/reply-heterozygous-pink1-p-g411s-in-rapid-eye-movement-sleep-behaviour-disorder
#17
Andreas Puschmann, Fabienne C Fiesel, Thomas R Caulfield, Roman Hudec, Maya Ando, Dominika Truban, Xu Hou, Kotaro Ogaki, Michael G Heckman, Elle D James, Maria Swanberg, Itzia Jimenez-Ferrer, Oskar Hansson, Grzegorz Opala, Joanna Siuda, Magdalena Boczarska-Jedynak, Andrzej Friedman, Dariusz Koziorowski, Monika Rudzinska-Bar, Jan O Aasly, Timothy Lynch, George D Mellick, Megha Mohan, Peter A Silburn, Yanosh Sanotsky, Carles Vilariño-Güell, Matthew J Farrer, Li Chen, Valina L Dawson, Ted M Dawson, Zbigniew K Wszolek, Owen A Ross, Wolfdieter Springer
No abstract text is available yet for this article.
March 29, 2017: Brain: a Journal of Neurology
https://www.readbyqxmd.com/read/28379291/heterozygous-pink1-p-g411s-in-rapid-eye-movement-sleep-behaviour-disorder
#18
Ziv Gan-Or, Jennifer A Ruskey, Dan Spiegelman, Isabelle Arnulf, Yves Dauvilliers, Birgit Högl, Christelle Monaca-Charley, Ronald B Postuma, Jacques Y Montplaisir, Guy A Rouleau
No abstract text is available yet for this article.
March 29, 2017: Brain: a Journal of Neurology
https://www.readbyqxmd.com/read/28368777/pink1-and-becn1-relocalize-at-mitochondria-associated-membranes-during-mitophagy-and-promote-er-mitochondria-tethering-and-autophagosome-formation
#19
Vania Gelmetti, Priscilla De Rosa, Liliana Torosantucci, Elettra Sara Marini, Alessandra Romagnoli, Martina Di Rienzo, Giuseppe Arena, Domenico Vignone, Gian Maria Fimia, Enza Maria Valente
Mitophagy is a highly specialized process to remove dysfunctional or superfluous mitochondria through the macroautophagy/autophagy pathway, aimed at protecting cells from the damage of disordered mitochondrial metabolism and apoptosis induction. PINK1, a neuroprotective protein mutated in autosomal recessive Parkinson disease, has been implicated in the activation of mitophagy by selectively accumulating on depolarized mitochondria, and promoting PARK2/Parkin translocation to them. While these steps have been characterized in depth, less is known about the process and site of autophagosome formation upon mitophagic stimuli...
April 3, 2017: Autophagy
https://www.readbyqxmd.com/read/28367808/-role-of-mitophagy-in-the-mitochondrial-quality-control
#20
Pierre Vigié, Nadine Camougrand
Mitochondria are highly dynamic organelles that provide essential metabolic functions and represent the major bioenergetic hub of eukaryotic cells. Mitochondrial dysfunctions are implicated in numerous diseases. Therefore, maintenance of a healthy pool of mitochondria is required for cellular function and survival. Mitochondrial quality control is achieved through several mechanisms that act at different levels: proteases and chaperones, the Ubiquitin-Proteasome-System (UPS) and mitophagy. Multiple mitophagy-involved programs operate independently or undergo crosstalk, and require modulated receptor activities at the outer membranes of mitochondria...
March 2017: Médecine Sciences: M/S
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