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https://www.readbyqxmd.com/read/28716706/characterization-of-a-presymptomatic-stage-in-a-drosophila-parkinson-s-disease-model-unveiling-dopaminergic-compensatory-mechanisms
#1
Daniela Molina-Mateo, Nicolás Fuenzalida-Uribe, Sergio Hidalgo, Claudia Molina-Fernández, Jorge Abarca, Rafaella V Zárate, Marcela Escandón, Reinaldo Figueroa, María Florencia Tevy, Jorge M Campusano
Parkinson disease (PD) is a degenerative disorder characterized by several motor symptoms including shaking, rigidity, slow movement and difficult walking, which has been associated to the death of nigro-striatal dopaminergic neurons. >90% of PD patients also present olfactory dysfunction. Although the molecular mechanisms responsible for this disease are not clear, hereditary PD is linked to mutations in specific genes, including the PTEN-induced putative kinase 1 (PINK1). In this work we provide for the first time a thorough temporal description of the behavioral effects induced by a mutation in the PINK1 gene in adult Drosophila, a previously described animal model for PD...
July 14, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28716427/influence-of-l-dopa-on-subtle-motor-signs-in-heterozygous-parkin-and-pink1-mutation-carriers
#2
Anne Weissbach, Inke R König, Katja Hückelheim, Peter P Pramstaller, Elisa Werner, Norbert Brüggemann, Vera Tadic, Katja Lohmann, Tobias Bäumer, Alexander Münchau, Meike Kasten, Christine Klein
INTRODUCTION: A latent nigrostriatal deficit and its possible clinical consequences in asymptomatic heterozygous Parkin and PINK1 mutation carriers (AMC) have been a matter of investigation in recent years. Notably, mild Parkinsonian signs in heterozygous mutation carriers can be so subtle that they may be missed if not specifically investigated. METHODS: We studied 15 heterozygous Parkin and PINK1 AMC and 18 age- and sex-matched mutation-negative controls using a standardized video, instructing the probands to perform relevant parts of the UPDRS III to investigate fine motor movements at baseline and after first-time L-Dopa administration...
July 8, 2017: Parkinsonism & related Disorders
https://www.readbyqxmd.com/read/28716221/parkin-mutation-may-be-associated-with-serious-akinesia-in-a-patient-with-parkinson-s-disease
#3
Yuto Uchihara, Hiroshi Kataoka, Hiroyo Yoshino, Ryogo Syobatake, Nobutaka Hattori, Satoshi Ueno
Acute akinesia (AA) is an unusual motor complication in Parkinson's disease (PD). Reported risk factors for AA include infection, trauma, surgical intervention, and the withdrawal of antiparkinsonian medication. Recently, patients with genetic PD were reported to have a three-fold risk of AA than patients with non-genetic PD. We describe a patient with PD associated with a Parkin mutation in whom serious akinesia developed. A 42-year-old man with exon 2 heterozygous deletion and exon 4 heterozygous deletion in the PARK2 gene showed five unexpected AA for several 12h...
August 15, 2017: Journal of the Neurological Sciences
https://www.readbyqxmd.com/read/28698153/curcumin-prevents-cisplatin-induced-renal-alterations-in-mitochondrial-bioenergetics-and-dynamic
#4
Bibiana Ortega-Domínguez, Omar Emiliano Aparicio-Trejo, Fernando E García-Arroyo, Juan Carlos León-Contreras, Edilia Tapia, Eduardo Molina-Jijón, Rogelio Hernández-Pando, Laura Gabriela Sánchez-Lozada, Diana Barrera-Oviedo, José Pedraza-Chaverri
Cisplatin is widely used as chemotherapeutic agent for treatment of diverse types of cancer, however, acute kidney injury (AKI) is an important side effect of this treatment. Diverse mechanisms have been involved in cisplatin-induced AKI, such as oxidative stress, apoptosis and mitochondrial damage. On the other hand, curcumin is a polyphenol extracted from the rhizome of Curcuma longa L. Previous studies have shown that curcumin protects against the cisplatin-induced AKI; however, it is unknown whether curcumin can reduce alterations in mitochondrial bioenergetics and dynamic in this model...
July 8, 2017: Food and Chemical Toxicology
https://www.readbyqxmd.com/read/28689991/ubiquitin-phosphorylated-at-ser57-hyper-activates-parkin
#5
Susanna George, Sabrina M Wang, Yumin Bi, Margot Treidlinger, Kathryn R Barber, Gary S Shaw, Patrick O'Donoghue
Malfunction of the ubiquitin (Ub) E3 ligase, parkin, leads to defects in mitophagy and protein quality control linked to Parkinson's disease. Parkin activity is stimulated by phosphorylation of Ub at Ser65 (pUb(S65)). Since the upstream kinase is only known for Ser65 (PINK1), the biochemical function of other phosphorylation sites on Ub remain largely unknown. We used fluorescently labelled and site-specifically phosphorylated Ub substrates to quantitatively relate the position and stoichiometry of Ub phosphorylation to parkin activation...
July 6, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28685977/the-post-therapeutic-effect-of-rapamycin-in-mild-traumatic-brain-injured-rats-ensuing-in-the-upregulation-of-autophagy-and-mitophagy
#6
Changxing Wang, Zhiying Hu, Yang Zou, Mingjun Xiang, Yuting Jiang, Benson O A Botchway, Xue Huo, Xiaoxue Du, Marong Fang
Mild traumatic brain injury (mTBI), common in juveniles, has been reported to be caused by sports-related concussion. Many young children may suffer from post-concussion syndrome. mTBI, in early stages of life, could play a part in neuron apoptosis and degeneration, cognitive and motor coordination impairment, as well as dementia. Our study was aimed at further investigating the post therapeutic efficacy of rapamycin in the recuperation of mTBI whiles at the same time investigating the metamorphosis in both autophagy and mitophagy in mTBI...
July 7, 2017: Cell Biology International
https://www.readbyqxmd.com/read/28684172/efficient-prevention-of-neurodegenerative-diseases-by-depletion-of-starvation-response-factor-ataxin-2
#7
REVIEW
Georg Auburger, Nesli-Ece Sen, David Meierhofer, Ayşe-Nazlı Başak, Aaron D Gitler
Ataxin-2 (ATXN2) homologs exist in all eukaryotic organisms and may have contributed to their origin. Apart from a role in endocytosis, they are known for global effects on mRNA repair and ribosomal translation. Cell size, protein synthesis, and fat and glycogen storage are repressed by ATXN2 via mTORC1 signaling. However, specific liver mitochondrial matrix enzymes and the mitochondrial repair factor PINK1 require ATXN2 abundance. During periods of starvation, ATXN2 is transcriptionally induced and localized to cytosolic stress granules, where nuclear factors dock to compensate RNA pathology...
July 3, 2017: Trends in Neurosciences
https://www.readbyqxmd.com/read/28683321/the-ubiquitination-of-pink1-is-restricted-to-its-mature-52-kda-form
#8
Yuhui Liu, Cristina Guardia-Laguarta, Jiang Yin, Hediye Erdjument-Bromage, Brittany Martin, Michael James, Xuejun Jiang, Serge Przedborski
Along with Parkin, PINK1 plays a critical role in maintaining mitochondrial quality control. Although PINK1 is expressed constitutively, its level is kept low in healthy mitochondria by polyubiquitination and ensuing proteasomal degradation of its mature, 52 kDa, form. We show here that the target of PINK1 polyubiquitination is the mature form and is mediated by ubiquitination of a conserved lysine at position 137. Notably, the full-length protein also contains Lys-137 but is not ubiquitinated. On the basis of our data, we propose that cleavage of full-length PINK1 at Phe-104 disrupts the major hydrophobic membrane-spanning domain in the protein, inducing a conformation change in the resultant mature form that exposes Lys-137 to the cytosol for subsequent modification by the ubiquitination machinery...
July 5, 2017: Cell Reports
https://www.readbyqxmd.com/read/28681509/akt2-ablation-prolongs-life-span-and-improves-myocardial-contractile-function-with-adaptive-cardiac-remodeling-role-of-sirt1-mediated-autophagy-regulation
#9
Jun Ren, Lifang Yang, Li Zhu, Xihui Xu, Asli F Ceylan, Wei Guo, Jian Yang, Yingmei Zhang
Aging is accompanied with unfavorable geometric and functional changes in the heart involving dysregulation of Akt and autophagy. This study examined the impact of Akt2 ablation on life span and cardiac aging as well as the mechanisms involved with a focus on autophagy and mitochondrial integrity. Cardiac geometry, contractile, and intracellular Ca(2+) properties were evaluated using echocardiography, IonOptix(®) edge-detection and fura-2 techniques. Levels of Sirt1, mitochondrial integrity, autophagy, and mitophagy markers were evaluated using Western blot...
July 5, 2017: Aging Cell
https://www.readbyqxmd.com/read/28673964/sorafenib-targets-the-mitochondrial-electron-transport-chain-complexes-and-atp-synthase-to-activate-the-pink1-parkin-pathway-and-modulate-cellular-drug-response
#10
Conggang Zhang, Zeyu Liu, Eric Bunker, Adrian Ramirez, Schuyler Lee, Yinghua Peng, Aik Choon Tan, S Gail Eckhardt, Douglas A Chapnick, Xuedong Liu
Sorafenib (Nexavar) is a broad-spectrum multi-kinase inhibitor that proves effective in treating advanced renal-cell carcinoma and liver cancer. Despite its well-characterized mechanism of action on several established cancer-related protein kinases, sorafenib causes variable responses among human tumors, although the cause for this variation is unknown. In an unbiased screening of an oncology drug library, we found that sorafenib activates recruitment of the ubiquitin E3 ligase Parkin to damaged mitochondria...
July 3, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28663346/pink1-and-parkin-regulate-drosophila-intestinal-stem-cell-proliferation-during-stress-and-aging
#11
Christopher L Koehler, Guy A Perkins, Mark H Ellisman, D Leanne Jones
Intestinal stem cells (ISCs) maintain the midgut epithelium in Drosophila melanogaster Proper cellular turnover and tissue function rely on tightly regulated rates of ISC division and appropriate differentiation of daughter cells. However, aging and epithelial injury cause elevated ISC proliferation and decreased capacity for terminal differentiation of daughter enteroblasts (EBs). The mechanisms causing functional decline of stem cells with age remain elusive; however, recent findings suggest that stem cell metabolism plays an important role in the regulation of stem cell activity...
June 29, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28661534/foxo3-promoted-mitophagy-via-nuclear-retention-induced-by-manganese-chloride-in-sh-sy5y-cells
#12
Dongmei Song, Junxiang Ma, Li Chen, Caixia Guo, Yuanyuan Zhang, Tian Chen, Shixuan Zhang, Zhonghui Zhu, Lin Tian, Piye Niu
OBJECTIVES: To evaluate the role of FOXO3 during the process of mitophagy induced by manganese chloride (MnCl2), mitochondrial dysfunction and mitophagy were detected before and after FOXO3 was knocked down in SH-SY5Y cells. METHOD: Transmission electron microscopy (TEM), flow cytometry, confocal microscopy and a western blot were used to detect mitochondrial ultrastructure and autophagy, Ca(2+) levels, mitochondrial reactive oxygen species (ROS) and the mitochondrial membrane potential (MMP), autophagosomes and mitophagy marker proteins (p62, LC3-II/LC3-I, Beclin-1, PINK1 and P-parkin), respectively...
June 29, 2017: Metallomics: Integrated Biometal Science
https://www.readbyqxmd.com/read/28647367/mitochondrial-quality-control-pathways-pink1-acts-as-a-gatekeeper
#13
Elvira P Leites, Vanessa A Morais
Mitochondria have a pivotal role in the maintenance of cell homeostasis and survival. Mitochondria are involved in processes such as ATP production, reactive oxygen species production, apoptosis induction, calcium homeostasis and protein degradation. Thus, mechanisms that regulate the intrinsic quality of mitochondria have a crucial role in dictating overall cell fate. The importance of these well-regulated mechanisms is highlighted in disease scenarios such as neurodegeneration, cancer and neuromuscular atrophy...
June 21, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28646096/heat-stress-causes-dysfunctional-autophagy-in-oxidative-skeletal-muscle
#14
Alexandra J Brownstein, Shanthi Ganesan, Corey M Summers, Sarah Pearce, Benjamin J Hale, Jason W Ross, Nicholas Gabler, Jacob T Seibert, Robert P Rhoads, Lance H Baumgard, Joshua T Selsby
We have previously established that 24 h of environmental hyperthermia causes oxidative stress and have implicated mitochondria as likely contributors to this process. Given this, we hypothesized that heat stress would lead to increased autophagy/mitophagy and a reduction in mitochondrial content. To address this hypothesis pigs were housed in thermoneutral (TN; 20°C) or heat stress (35°C) conditions for 1- (HS1) or 3- (HS3) days and the red and white portions of the semitendinosus collected. We did not detect differences in glycolytic muscle...
June 2017: Physiological Reports
https://www.readbyqxmd.com/read/28641777/role-of-parl-pink1-parkin-pathway-in-adipocyte-differentiation
#15
Ming-Yuh Shiau, Pin-Shen Lee, Ying-Jyun Huang, Ching-Ping Yang, Chiao-Wan Hsiao, Kai-Yun Chang, Huan-Wen Chen, Yih-Hsin Chang
OBJECTIVE: Adipogenesis determines the number of adipocytes which is increased when individuals become obese. Mitochondria undergo remarkable morphological and functional changes during adipogenesis. PTEN-induced kinase 1 (PINK1) is pivotal to maintain mitochondrial homeostasis in neural cells. The present study aimed at investigating effects of PINK1 on adipogenesis and energy metabolism. METHODS: Expression of presenilin associated rhomboid-like protein (PARL), PINK1 and Parkin, as well as the interaction among these proteins was temporally examined during adipogenesis...
July 2017: Metabolism: Clinical and Experimental
https://www.readbyqxmd.com/read/28620835/twenty-years-since-the-discovery-of-the-parkin-gene
#16
REVIEW
Nobutaka Hattori, Yoshikuni Mizuno
Nearly 20 years have passed since we identified the causative gene for a familial Parkinson's disease, parkin (now known as PARK2), in 1998. PARK2 is the most common gene responsible for young-onset Parkinson's disease. It codes for the protein Parkin RBR E3 ubiquitin-protein ligase (PARK2), which directly links to the ubiquitin-proteasome as a ubiquitin ligase. PARK2 is involved in mitophagy, which is a type of autophagy, in collaboration with PTEN-induced putative kinase 1 (PINK1). The PINK1 gene (previously known as PARK6) is also a causative gene for young-onset Parkinson's disease...
June 15, 2017: Journal of Neural Transmission
https://www.readbyqxmd.com/read/28618992/modulating-mitophagy-in-mitochondrial-disease
#17
Eszter Dombi, Heather Mortiboys, Joanna Poulton
Mitochondrial diseases may result from mutations in the maternally-inherited mitochondrial DNA (mtDNA) or from mutations in nuclear genes encoding mitochondrial proteins. Their bi-genomic nature makes mitochondrial diseases a very heterogeneous group of disorders that can present at any age and can affect any type of tissue. The autophagic-lysosomal degradation pathway plays an important role in clearing dysfunctional and redundant mitochondria through a specific quality control mechanism termed mitophagy. Mitochondria could be targeted for autophagic degradation for a variety of reasons including basal turnover for recycling, starvation induced degradation, and degradation due to damage...
June 16, 2017: Current Medicinal Chemistry
https://www.readbyqxmd.com/read/28615325/calcium-calmodulin-dependent-protein-kinase-regulates-the-pink1-parkin-and-dj-1-pathways-of-mitophagy-during-sepsis
#18
Xianghong Zhang, Du Yuan, Qian Sun, Li Xu, Emma Lee, Anthony J Lewis, Brian S Zuckerbraun, Matthew R Rosengart
During sepsis and shock states, mitochondrial dysfunction occurs. Consequently, adaptive mechanisms, such as fission, fusion, and mitophagy, are induced to eliminate damaged portions or entire dysfunctional mitochondria. The regulatory PINK1/Parkin and DJ-1 pathways are strongly induced by mitochondrial depolarization, although a direct link between loss of mitochondrial membrane potential (ΔΨ) and mitophagy has not been identified. Mitochondria also buffer Ca(2+), and their buffering capacity is dependent on ΔΨ...
June 14, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/28608965/hydrogen-sulphide-modulating-mitochondrial-morphology-to-promote-mitophagy-in-endothelial-cells-under-high-glucose-and-high-palmitate
#19
Ning Liu, Jichao Wu, Linxue Zhang, Zhaopeng Gao, Yu Sun, Miao Yu, Yajun Zhao, Shiyun Dong, Fanghao Lu, Weihua Zhang
Endothelial cell dysfunction is one of the main reasons for type II diabetes vascular complications. Hydrogen sulphide (H2 S) has antioxidative effect, but its regulation on mitochondrial dynamics and mitophagy in aortic endothelial cells under hyperglycaemia and hyperlipidaemia is unclear. Rat aortic endothelial cells (RAECs) were treated with 40 mM glucose and 200 μM palmitate to imitate endothelium under hyperglycaemia and hyperlipidaemia, and 100 μM NaHS was used as an exogenous H2 S donor. Firstly, we demonstrated that high glucose and palmitate decreased H2 S production and CSE expression in RAECs...
June 13, 2017: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/28602540/deficiencies-in-mitochondrial-dynamics-sensitize-caenorhabditis-elegans-to-arsenite-and-other-mitochondrial-toxicants-by-reducing-mitochondrial-adaptability
#20
Anthony L Luz, Tewodros R Godebo, Latasha L Smith, Tess C Leuthner, Laura L Maurer, Joel N Meyer
Mitochondrial fission, fusion, and mitophagy are interlinked processes that regulate mitochondrial shape, number, and size, as well as metabolic activity and stress response. The fundamental importance of these processes is evident in the fact that mutations in fission (DRP1), fusion (MFN2, OPA1), and mitophagy (PINK1, PARK2) genes can cause human disease (collectively >1/10,000). Interestingly, however, the age of onset and severity of clinical manifestations varies greatly between patients with these diseases (even those harboring identical mutations), suggesting a role for environmental factors in the development and progression of certain mitochondrial diseases...
June 8, 2017: Toxicology
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