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https://www.readbyqxmd.com/read/29142257/using-a-quantitative-quadruple-immunofluorescent-assay-to-diagnose-isolated-mitochondrial-complex-i-deficiency
#1
Syeda T Ahmed, Charlotte L Alston, Sila Hopton, Langping He, Iain P Hargreaves, Gavin Falkous, Monika Oláhová, Robert McFarland, Doug M Turnbull, Mariana C Rocha, Robert W Taylor
Isolated Complex I (CI) deficiency is the most commonly observed mitochondrial respiratory chain biochemical defect, affecting the largest OXPHOS component. CI is genetically heterogeneous; pathogenic variants affect one of 38 nuclear-encoded subunits, 7 mitochondrial DNA (mtDNA)-encoded subunits or 14 known CI assembly factors. The laboratory diagnosis relies on the spectrophotometric assay of enzyme activity in mitochondrially-enriched tissue homogenates, requiring at least 50 mg skeletal muscle, as there is no reliable histochemical method for assessing CI activity directly in tissue cryosections...
November 15, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29139328/repression-of-oxidative-phosphorylation-sensitizes-leukemia-cell-lines-to-cytarabine
#2
Burcu Yucel, Mehmet Sonmez
OBJECTIVES: Leukemia is a group of bone marrow cancers and drug resistance is one of the challenges in treatment. Caffeic acid phenethyl ester's (CAPE's) anti-proliferative and apoptotic properties have been reported in leukemia cell lines. However, CAPE's effect on drug resistance and cellular metabolism is still unknown. Thus, in this study, we aimed to explore CAPE's effect on drug resistance and oxidative phosphorylation (oxphos). METHODS: Leukemia cell lines NB-4, HL-60, and K562 were treated with CAPE...
November 15, 2017: Hematology (Amsterdam, Netherlands)
https://www.readbyqxmd.com/read/29138224/short-term-metformin-and-exercise-training-effects-on-strength-aerobic-capacity-glycemic-control-and-mitochondrial-function-in-children-with-burn-injury
#3
Eric Rivas, David N Herndon, Craig Porter, Walter Meyer, Oscar E Suman
Severely burned children experience a chronic state of sympathetic nervous system activation that is associated with hypermetabolic/cardiac stress and muscle wasting. Metformin, a diabetes medication, helps control hyperglycemia in diabetic populations, and exercise has been shown to improve exercise strength and aerobic exercise capacity after severe burns. However, whether exercise improves glycemic control in burned children and whether combining exercise and metformin improves outcomes to a greater degree than exercise alone is unknown...
November 14, 2017: American Journal of Physiology. Endocrinology and Metabolism
https://www.readbyqxmd.com/read/29137472/changes-in-transcription-pattern-lead-to-a-marked-decrease-in-cox-cs-and-sqr-activity-after-the-developmental-point-of-the-22-nd-gestational-week
#4
H Kolarova, J Krizova, M Hulkova, H Hansikova, H Hulkova, V Smid, J Zeman, T Honzik, M Tesarova
Tissue differentiation and proliferation throughout fetal development interconnect with changes in the Oxidative Phosphorylation System (OXPHOS) on the cellular level. Reevaluation of the expression data revealed a significant increase in COX4 and MTATP6 liver transcription levels after the 22(nd) gestational week (GW) which inspired us to characterize its functional impact. Specific activities of cytochrome c oxidase (COX), citrate synthase (CS), succinate-coenzyme Q reductase (SQR) and mtDNA determined by spectrophotometry and RT-PCR were studied in a set of 25 liver and 18 skeletal muscle samples at 13(th) to 29(th) GW...
November 10, 2017: Physiological Research
https://www.readbyqxmd.com/read/29132502/transcriptomic-and-proteomic-landscape-of-mitochondrial-dysfunction-reveals-secondary-coenzyme-q-deficiency-in-mammals
#5
Inge Kühl, Maria Miranda, Ilian Atanassov, Irina Kuznetsova, Yvonne Hinze, Arnaud Mourier, Aleksandra Filipovska, Nils-Göran Larsson
Dysfunction of the oxidative phosphorylation (OXPHOS) system is a major cause of human disease and the cellular consequences are highly complex. Here, we present comparative analyses of mitochondrial proteomes, cellular transcriptomes and targeted metabolomics of five knockout mouse strains deficient in essential factors required for mitochondrial DNA gene expression, leading to OXPHOS dysfunction. Moreover, we describe sequential protein changes during post-natal development and progressive OXPHOS dysfunction in time course analyses in control mice and a middle lifespan knockout, respectively...
November 14, 2017: ELife
https://www.readbyqxmd.com/read/29127235/cardiac-performance-is-limited-by-oxygen-delivery-to-the-mitochondria-in-the-crystalloid-perfused-working-heart
#6
Sarah Kuzmiak-Glancy, Raul Covian, Armel N Femnou, Brian Glancy, Rafael Jaimes, Anastasia M Wengrowski, Kara Garrott, Stephanie French, Robert S Balaban, Matthew W Kay
The left ventricular (LV) working, crystalloid-perfused heart is used extensively to evaluate basic cardiac function, pathophysiology, and pharmacology. Crystalloid-perfused hearts may be limited by oxygen delivery, as adding oxygen carriers increases myoglobin oxygenation and improves myocardial function. However, whether decreased myoglobin oxygen saturation impacts oxidative phosphorylation (OxPhos) is unresolved since myoglobin has a much lower affinity for oxygen than cytochrome c oxidase (COX). In the present study, a laboratory-based synthesis of an affordable perfluorocarbon (PFC) emulsion was developed to increase perfusate oxygen-carrying capacity without impeding optical absorbance assessments...
November 10, 2017: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/29120753/mitochondrial-oxphos-induced-by-rb1-deficiency-in-breast-cancer-implications-for-anabolic-metabolism-stemness-and-metastasis
#7
REVIEW
Eldad Zacksenhaus, Mariusz Shrestha, Jeff C Liu, Ioulia Vorobieva, Philip E D Chung, YoungJun Ju, Uri Nir, Zhe Jiang
A switch from catabolic to anabolic metabolism, a major hallmark of cancer, enables rapid cell duplication, and is driven by multiple oncogenic alterations, including PIK3CA mutation, MYC amplification, and TP53 loss. However, tumor growth requires active mitochondrial function and oxidative phosphorylation (OXPHOS). Recently, loss of the retinoblastoma (RB1) tumor suppressor in breast cancer was shown to induce mitochondrial protein translation (MPT) and OXPHOS. Here, we discuss how increased OXPHOS can enhance anabolic metabolism and cell proliferation, as well as cancer stemness and metastasis...
November 2017: Trends in Cancer
https://www.readbyqxmd.com/read/29120065/biallelic-mutations-in-mitochondrial-tryptophanyl-trna-synthetase-cause-levodopa-rresponsive-infantile-onset-parkinsonism
#8
E A Burke, S J Frucht, K Thompson, L A Wolfe, T Yokoyama, M Bertoni, Y Huang, M Sincan, D R Adams, R W Taylor, W A Gahl, C Toro, M C V Malicdan
Mitochondrial aminoacyl-tRNA synthetases (mtARSs) are essential, ubiquitously expressed enzymes that covalently attach amino acids to their corresponding tRNA molecules during translation of mitochondrial genes. Deleterious variants in the mtARS genes cause a diverse array of phenotypes, many of which involve the nervous system. Moreover, distinct mutations in mtARSs often cause different clinical manifestations. Recently, the gene encoding mitochondrial tryptophanyl tRNA synthetase (WARS2) was reported to cause two different neurological phenotypes, a form of autosomal recessive intellectual disability and a syndrome of severe infantile-onset leukoencephalopathy...
November 9, 2017: Clinical Genetics
https://www.readbyqxmd.com/read/29119535/mitochondria-bound-hexokinase-mt-hk-activity-differ-in-cortical-and-hypothalamic-synaptosomes-differential-role-of-mt-hk-in-h2o2-depuration
#9
João Paulo Cavalcanti-de-Albuquerque, Eduardo de Souza Ferreira, Denise Pires de Carvalho, Antonio Galina
Glucose and oxygen are vital for the brain, as these molecules provide energy and metabolic intermediates that are necessary for cell function. The glycolysis pathway and mitochondria play a pivotal role in cell energy metabolism, which is closely related to reactive oxygen species (ROS) production. Hexokinase (HK) is a key enzyme involved in glucose metabolism that modulates the level of brain mitochondrial ROS by recycling ADP for oxidative phosphorylation (OxPhos). Here, we hypothesize that the control of mitochondrial metabolism by hexokinase differs in distinct areas of the brain, such as the cortex and hypothalamus, in which ROS might function as signaling molecules...
November 8, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/29118086/creb-crtc2-controls-glp-1-dependent-regulation-of-glucose-homeostasis
#10
Ji-Hyun Lee, Xianlan Wen, Hana Cho, Seung-Hoi Koo
Glucagon-like peptide 1 (GLP-1) is a major incretin that controls glucose homeostasis. The secretion of mature GLP-1 is regulated via GPCRs, including bile acid receptor G protein-coupled bile acid receptor 1, which uses cAMP signaling to enhance the exocytosis of GLP-1-containing vesicles. However, the role of cAMP-mediated transcription has not been clearly demonstrated to date. In this study, we explored the role of cAMP response element-binding protein/CREB-regulated transcription coactivator 2 (CREB/CRTC2)-dependent transcription on GLP-1 secretion in the L cells...
November 8, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/29117544/glial-cell-evolution-the-origins-of-a-lipid-store
#11
Klaus-Armin Nave, Iva D Tzvetanova, Stefanie Schirmeier
In Drosophila, neuronal mitochondria that lack OXPHOS generate ROS-protective fatty acids and lipid droplets in associated glia. In this issue, Liu et al. (2017) demonstrate that neuronal lipid synthesis is driven by the glial lactate shuttle. This lipoprotein-dependent deposition of lipids may be at the origin of glial specializations evolving in vertebrates.
November 7, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/29109251/metabolic-control-of-regulatory-t-cell-treg-survival-and-function-by-lkb1
#12
Nanhai He, Weiwei Fan, Brian Henriquez, Ruth T Yu, Annette R Atkins, Christopher Liddle, Ye Zheng, Michael Downes, Ronald M Evans
The metabolic programs of functionally distinct T cell subsets are tailored to their immunologic activities. While quiescent T cells use oxidative phosphorylation (OXPHOS) for energy production, and effector T cells (Teffs) rely on glycolysis for proliferation, the distinct metabolic features of regulatory T cells (Tregs) are less well established. Here we show that the metabolic sensor LKB1 is critical to maintain cellular metabolism and energy homeostasis in Tregs. Treg-specific deletion of Lkb1 in mice causes loss of Treg number and function, leading to a fatal, early-onset autoimmune disorder...
November 6, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29103922/17%C3%AE-estradiol-directly-lowers-mitochondrial-membrane-microviscosity-and-improves-bioenergetic-function-in-skeletal-muscle
#13
Maria J Torres, Kim A Kew, Terence E Ryan, Edward Ross Pennington, Chien-Te Lin, Katherine A Buddo, Amy M Fix, Cheryl A Smith, Laura A Gilliam, Sira Karvinen, Dawn A Lowe, Espen E Spangenburg, Tonya N Zeczycki, Saame Raza Shaikh, P Darrell Neufer
Menopause results in a progressive decline in 17β-estradiol (E2) levels, increased adiposity, decreased insulin sensitivity, and a higher risk for type 2 diabetes. Estrogen therapies can help reverse these effects, but the mechanism(s) by which E2 modulates susceptibility to metabolic disease is not well understood. In young C57BL/6N mice, short-term ovariectomy decreased-whereas E2 therapy restored-mitochondrial respiratory function, cellular redox state (GSH/GSSG), and insulin sensitivity in skeletal muscle...
November 1, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/29103101/ischemic-preconditioning-protects-astrocytes-against-oxygen-glucose-deprivation-via-the-nuclear-erythroid-2-related-factor-2-pathway
#14
Srinivasan V Narayanan, Kunjan R Dave, Miguel A Perez-Pinzon
Induction of ischemic preconditioning (IPC) represents a potential therapy against cerebral ischemia by activation of adaptive pathways and modulation of mitochondria to induce ischemic tolerance to various cells and tissues. Mitochondrial dysfunction has been ascribed to contribute to numerous neurodegenerative conditions and cerebral ischemia. Nuclear erythroid 2-related factor 2 (Nrf2) is a transcription factor that has traditionally been involved in upregulating cellular antioxidant systems to combat oxidative stress in the brain; however, the association of Nrf2 with mitochondria in the brain remains unclear...
November 4, 2017: Translational Stroke Research
https://www.readbyqxmd.com/read/29101324/cyclophilin-d-regulates-the-dynamic-assembly-of-mitochondrial-atp-synthase-into-synthasomes
#15
Gisela Beutner, Ryan E Alanzalon, George A Porter
Mitochondrial electron transport is essential for oxidative phosphorylation (OXPHOS). Electron transport chain (ETC) activity generates an electrochemical gradient that is used by the ATP synthase to make ATP. ATP synthase is organized into supramolecular units called synthasomes that increase the efficiency of ATP production, while within ATP synthase is the cyclophilin D (CypD) regulated mitochondrial permeability transition pore (PTP). We investigated whether synthasomes are dynamic structures that respond to metabolic demands and whether CypD regulates this dynamic...
November 3, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29099651/nutritional-interventions-for-mitochondrial-oxphos-deficiencies-mechanisms-and-model-systems
#16
Adam J Kuszak, Michael Graham Espey, Marni J Falk, Marissa A Holmbeck, Giovanni Manfredi, Gerald S Shadel, Hilary J Vernon, Zarazuela Zolkipli-Cunningham
Multisystem metabolic disorders caused by defects in oxidative phosphorylation (OXPHOS) are severe and often lethal, conditions. Inborn errors of OXPHOS function are termed primary mitochondrial disorders (PMDs), and the use of nutritional interventions is routine in their supportive management. However, detailed mechanistic understanding and evidence for efficacy and safety of these interventions are limited. Preclinical cellular and animal model systems are important tools to investigate PMD metabolic mechanisms and therapeutic strategies...
November 3, 2017: Annual Review of Pathology
https://www.readbyqxmd.com/read/29099268/atm-mediated-mitochondrial-damage-response-triggered-by-nuclear-dna-damage-in-normal-human-lung-fibroblasts
#17
Tsutomu Shimura, Megumi Sasatani, Hidehiko Kawai, Kenji Kamiya, Junya Kobayashi, Kenshi Komatsu, Naoki Kunugita
Ionizing radiation (IR) elevates mitochondrial oxidative phosphorylation (OXPHOS) in response to the energy requirement for DNA damage responses. Reactive oxygen species (ROS) released during mitochondrial OXPHOS may cause oxidative damage to mitochondria in irradiated cells. In this paper, we investigated the association between nuclear DNA damage and mitochondrial damage following IR in normal human lung fibroblasts. In contrast to low-doses of acute single radiation, continuous exposure of chronic radiation or long-term exposure of fractionated radiation (FR) induced persistent Rad51 and γ-H2AX foci at least 24 hours after IR in irradiated cells...
November 3, 2017: Cell Cycle
https://www.readbyqxmd.com/read/29098465/a-metabolic-therapy-for-malignant-glioma-requires-a-clinical-measure
#18
REVIEW
Zachary Corbin, Daniel Spielman, Lawrence Recht
Cancers are "reprogrammed" to use a much higher rate of glycolysis (GLY) relative to oxidative phosphorylation (OXPHOS), even in the presence of adequate amounts of oxygenation. Originally identified by Nobel Laureate Otto Warburg, this hallmark of cancer has recently been termed metabolic reprogramming and represents a way for the cancer tissue to divert carbon skeletons to produce biomass. Understanding the mechanisms that underlie this metabolic shift should lead to better strategies for cancer treatments...
November 2, 2017: Current Oncology Reports
https://www.readbyqxmd.com/read/29093766/generation-and-bioenergetic-profiles-of-cybrids-with-east-asian-mtdna-haplogroups
#19
Huaibin Zhou, Ke Nie, Ruyi Qiu, Jingting Xiong, Xiaoli Shao, Bingqian Wang, Lijun Shen, Jianxin Lyu, Hezhi Fang
Human mitochondrial DNA (mtDNA) variants and haplogroups may contribute to susceptibility to various diseases and pathological conditions, but the underlying mechanisms are not well understood. To address this issue, we established a cytoplasmic hybrid (cybrid) system to investigate the role of mtDNA haplogroups in human disease; specifically, we examined the effects of East Asian mtDNA genetic backgrounds on oxidative phosphorylation (OxPhos). We found that mtDNA single nucleotide polymorphisms such as m.489T>C, m...
2017: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/29093663/selection-and-characterization-of-palmitic-acid-responsive-patients-with-an-oxphos-complex-i-defect
#20
Tom E J Theunissen, Mike Gerards, Debby M E I Hellebrekers, Florence H van Tienen, Rick Kamps, Suzanne C E H Sallevelt, Elvira N M M-D Hartog, Hans R Scholte, Robert M Verdijk, Kees Schoonderwoerd, Irenaeus F M de Coo, Radek Szklarczyk, Hubert J M Smeets
Mitochondrial disorders are genetically and clinically heterogeneous, mainly affecting high energy-demanding organs due to impaired oxidative phosphorylation (OXPHOS). Currently, effective treatments for OXPHOS defects, with complex I deficiency being the most prevalent, are not available. Yet, clinical practice has shown that some complex I deficient patients benefit from a high-fat or ketogenic diet, but it is unclear how these therapeutic diets influence mitochondrial function and more importantly, which complex I patients could benefit from such treatment...
2017: Frontiers in Molecular Neuroscience
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