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https://www.readbyqxmd.com/read/28646906/modulation-of-oxidative-phosphorylation-and-redox-homeostasis-in-mitochondrial-ndufs4-deficiency-via-mesenchymal-stem-cells
#1
Marlen Melcher, Katharina Danhauser, Annette Seibt, Özer Degistirici, Fabian Baertling, Arun Kumar Kondadi, Andreas S Reichert, Werner J H Koopman, Peter H G M Willems, Richard J Rodenburg, Ertan Mayatepek, Roland Meisel, Felix Distelmaier
BACKGROUND: Disorders of the oxidative phosphorylation (OXPHOS) system represent a large group among the inborn errors of metabolism. The most frequently observed biochemical defect is isolated deficiency of mitochondrial complex I (CI). No effective treatment strategies for CI deficiency are so far available. The purpose of this study was to investigate whether and how mesenchymal stem cells (MSCs) are able to modulate metabolic function in fibroblast cell models of CI deficiency. METHODS: We used human and murine fibroblasts with a defect in the nuclear DNA encoded NDUFS4 subunit of CI...
June 24, 2017: Stem Cell Research & Therapy
https://www.readbyqxmd.com/read/28646582/comprehensive-mathematical-model-of-oxidative-phosphorylation-valid-for-physiological-up-to-pathological-conditions
#2
Margit Heiske, Thierry Letellier, Edda Klipp
We developed a mathematical model of oxidative phosphorylation (OXPHOS) that allows for a precise description of mitochondrial function with respect to the respiratory flux and the ATP production. The model reproduced flux-force relationships under various experimental conditions (state 3 and 4, uncoupling, shortage of respiratory substrate) as well as time courses, exhibiting correct P/O ratios. The model was able to reproduce experimental threshold curves for perturbations of the respiratory chain complexes, the F1 F0 -ATP synthase, the ADP/ATP carrier, the phosphate/OH carrier, and the proton leak...
June 24, 2017: FEBS Journal
https://www.readbyqxmd.com/read/28624784/mitochondrial-pyruvate-carrier-function-determines-cell-stemness-and-metabolic-reprogramming-in-cancer-cells
#3
Xiaoli Li, Gaoyang Han, Xiaoran Li, Quancheng Kan, Zhirui Fan, Yaqing Li, Yasai Ji, Jing Zhao, Mingzhi Zhang, Mantas Grigalavicius, Viktor Berge, Mariusz Adam Goscinski, Jahn M Nesland, Zhenhe Suo
One of the remarkable features of cancer cells is aerobic glycolysis, a phenomenon known as the "Warburg Effect", in which cells rely preferentially on glycolysis instead of oxidative phosphorylation (OXPHOS) as the main energy source even in the presence of high oxygen tension. Cells with dysfunctional mitochondria are unable to generate sufficient ATP from mitochondrial OXPHOS, and then are forced to rely on glycolysis for ATP generation. Here we report our results in a prostate cancer cell line in which the mitochondrial pyruvate carrier 1 (MPC1) gene was knockout...
May 25, 2017: Oncotarget
https://www.readbyqxmd.com/read/28623342/hif-1%C3%AE-knockdown-reduces-glycolytic-metabolism-and-induces-cell-death-of-human-synovial-fibroblasts-under-normoxic-conditions
#4
Manuel J Del Rey, Álvaro Valín, Alicia Usategui, Carmen M García-Herrero, María Sánchez-Aragó, José M Cuezva, María Galindo, Beatriz Bravo, Juan D Cañete, Francisco J Blanco, Gabriel Criado, José L Pablos
Increased glycolysis and HIF-1α activity are characteristics of cells under hypoxic or inflammatory conditions. Besides, in normal O2 environments, elevated rates of glycolysis support critical cellular mechanisms such as cell survival. The purpose of this study was to analyze the contribution of HIF-1α to the energy metabolism and survival of human synovial fibroblasts (SF) under normoxic conditions. HIF-1α was silenced using lentiviral vectors or small-interfering RNA (siRNA) duplexes. Expression analysis by qRT-PCR and western blot of known HIF-1α target genes in hypoxia demonstrated the presence of functional HIF-1α in normoxic SF and confirmed the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH) as a HIF-1α target even in normoxia...
June 16, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28618997/vdac1-as-a-player-in-mitochondria-mediated-apoptosis-and-target-for-modulating-apoptosis
#5
Varda Shoshan-Barmatz, Yakov Krelin, Quan Chen
The voltage-dependent anion channel 1 (VDAC1), an outer mitochondria membrane protein, functions as a mitochondrial governor, controlling transport of metabolites in and out of the mitochondria and energy production, while also coordinating glycolysis and oxidative phosphorylation (OXPHOS). . VDAC1 plays a key role in mitochondria-mediated apoptosis by functioning in the release of apoptotic proteins located in the inter-membranal space (IMS) and due to its association with pro- and anti-apoptotic proteins...
June 16, 2017: Current Medicinal Chemistry
https://www.readbyqxmd.com/read/28616179/prediction-of-harmful-variants-on-mitochondrial-genes-test-of-habitat-dependent-and-demographic-effects-in-a-euryhaline-fish
#6
Anti Vasemägi, Janne Sulku, Matthieu Bruneaux, Olaf Thalmann, Hannu Mäkinen, Mikhail Ozerov
Both effective population size and life history may influence the efficacy of purifying selection, but it remains unclear if the environment affects the accumulation of weakly deleterious nonsynonymous polymorphisms. We hypothesize that the reduced energetic cost of osmoregulation in brackish water habitat may cause relaxation of selective constraints at mitochondrial oxidative phosphorylation (OXPHOS) genes. To test this hypothesis, we analyzed 57 complete mitochondrial genomes of Pungitius pungitius collected from brackish and freshwater habitats...
June 2017: Ecology and Evolution
https://www.readbyqxmd.com/read/28592294/exercise-in-claudicants-increase-or-decrease-walking-ability-and-the-response-relates-to-mitochondrial-function
#7
Michel van Schaardenburgh, Martin Wohlwend, Øivind Rognmo, Erney J R Mattsson
BACKGROUND: Exercise of patients with intermittent claudication improves walking performance. Exercise does not usually increase blood flow, but seems to increase muscle mitochondrial enzyme activities. Although exercise is beneficial in most patients, it might be harmful in some. The mitochondrial response to exercise might therefore differ between patients. Our hypothesis was that changes in walking performance relate to changes in mitochondrial function after 8 weeks of exercise. At a subgroup level, negative responders decrease and positive responders increase mitochondrial capacity...
June 7, 2017: Journal of Translational Medicine
https://www.readbyqxmd.com/read/28591857/adaptive-patterns-of-mitogenome-evolution-are-associated-with-the-loss-of-shell-scutes-in-turtles
#8
Tibisay Escalona, Cameron J Weadick, Agostinho Antunes
The mitochondrial genome encodes several protein components of the oxidative phosphorylation (OXPHOS) pathway and is critical for aerobic respiration. These proteins have evolved adaptively in many taxa, but linking molecular-level patterns with higher-level attributes (e.g., morphology, physiology) remains a challenge. Turtles are a promising system for exploring mitochondrial genome evolution as different species face distinct respiratory challenges and employ multiple strategies for ensuring efficient respiration...
June 6, 2017: Molecular Biology and Evolution
https://www.readbyqxmd.com/read/28591633/cytochrome-c-oxidase-activity-is-a-metabolic-checkpoint-that-regulates-cell-fate-decisions-during-t-cell-activation-and-differentiation
#9
Tatyana N Tarasenko, Susan E Pacheco, Mary Kay Koenig, Julio Gomez-Rodriguez, Senta M Kapnick, Francisca Diaz, Patricia M Zerfas, Emanuele Barca, Jessica Sudderth, Ralph J DeBerardinis, Raul Covian, Robert S Balaban, Salvatore DiMauro, Peter J McGuire
T cells undergo metabolic reprogramming with major changes in cellular energy metabolism during activation. In patients with mitochondrial disease, clinical data were marked by frequent infections and immunodeficiency, prompting us to explore the consequences of oxidative phosphorylation dysfunction in T cells. Since cytochrome c oxidase (COX) is a critical regulator of OXPHOS, we created a mouse model with isolated dysfunction in T cells by targeting a gene, COX10, that produces mitochondrial disease in humans...
June 6, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28585712/a-novel-non-apoptotic-role-of-procaspase-3-in-the-regulation-of-mitochondrial-biogenesis-activators
#10
Ji-Soo Kim, Ji-Young Ha, Sol-Ji Yang, Jin H Son
The executioner caspase-3 has been proposed as a pharmacological intervention target to preserve degenerating dopaminergic (DA) neurons because apoptotic mechanisms involving caspase-3 contribute, at least in part, to the loss of DA neurons in patients and experimental models of Parkinson's disease (PD). Here, we determined that genetic intervention of caspase-3 was sufficient to prevent cell death against oxidative stress (OS), accompanied by unexpected severe mitochondrial dysfunction. Specifically, as we expected, caspase-3-deficient DA neuronal cells were very significantly resistant to OS-induced cell death, while the activation of the initiator caspase-9 by OS was preserved...
June 6, 2017: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/28583467/leucine-reduces-reactive-oxygen-species-levels-via-an-energy-metabolism-switch-by-activation-of-the-mtor-hif-1%C3%AE-pathway-in-porcine-intestinal-epithelial-cells
#11
Jun Hu, Yangfan Nie, Shifeng Chen, Chunlin Xie, Qiwen Fan, Zhichang Wang, Baisheng Long, Guokai Yan, Qing Zhong, Xianghua Yan
Leucine serves not only as a substrate for protein synthesis, but also as a signal molecule involved in protein metabolism. However, whether the levels of cellular reactive oxygen species (ROS), which have damaging effects on cellular DNA, proteins, and lipids, are regulated by leucine is still unclear. Here, we report that leucine supplementation reduces ROS levels in intestinal epithelial cells of weaned piglets. A proteomics analysis revealed that leucine supplementation induces an energy metabolism switch from oxidative phosphorylation (OXPHOS) towards glycolysis...
June 2, 2017: International Journal of Biochemistry & Cell Biology
https://www.readbyqxmd.com/read/28580772/exercise-training-increases-skeletal-muscle-mitochondrial-volume-density-by-enlargement-of-existing-mitochondria-and-not-de-novo-biogenesis
#12
Anne-Kristine Meinild Lundby, Robert A Jacobs, Saskia Gehrig, Jeroen de Leur, Moritz Hauser, Thomas C Bonne, Daniela Flück, Sune Dandanell, Niels Kirk, Andreas Kaech, Urs Ziegler, Steen Larsen, Carsten Lundby
AIMS: 1) determine whether exercise induced increases in muscle mitochondrial volume density (MitoVD ) is related to enlargement of existing mitochondria or de novo biogenesis, 2) establish if measures of mitochondrial-specific enzymatic activities are valid biomarkers for exercise induced increases in MitoVD . METHOD: Skeletal muscle samples were collected from twenty-one healthy males prior to and following 6 weeks of endurance training. Transmission electron microscopy was used for estimation of mitochondrial densities and profiles...
June 5, 2017: Acta Physiologica
https://www.readbyqxmd.com/read/28575497/loss-of-hepatic-lrpprc-alters-mitochondrial-bioenergetics-regulation-of-permeability-transition-and-trans-membrane-ros-diffusion
#13
Alexanne Cuillerier, Shamisa Honarmand, Virgilio J J Cadete, Matthieu Ruiz, Anik Forest, Sonia Deschênes, Claudine Beauchamp, Guy Charron, John D Rioux, Christine Des Rosiers, Eric A Shoubridge, Yan Burelle
BACKGROUND AND AIMS: The French-Canadian variant of Leigh Syndrome (LSFC) is an autosomal recessive oxidative phosphorylation (OXPHOS) disorder caused by a mutation in LRPPRC, coding for a protein involved in the stability of mitochondrially-encoded mRNAs. Low levels of LRPPRC are present in all patient tissues, but result in a disproportionately severe OXPHOS defect in the brain and liver, leading to unpredictable subacute metabolic crises. METHODS: To investigate the impact of the OXPHOS defect in the liver, we analyzed the mitochondrial phenotype in mice harboring an hepatocyte-specific inactivation of Lrpprc...
May 31, 2017: Human Molecular Genetics
https://www.readbyqxmd.com/read/28558019/overexpression-of-the-human-dek-oncogene-reprograms-cellular-metabolism-and-promotes-glycolysis
#14
Marie C Matrka, Miki Watanabe, Ranjithmenon Muraleedharan, Paul F Lambert, Andrew N Lane, Lindsey E Romick-Rosendale, Susanne I Wells
The DEK oncogene is overexpressed in many human malignancies including at early tumor stages. Our reported in vitro and in vivo models of squamous cell carcinoma have demonstrated that DEK contributes functionally to cellular and tumor survival and to proliferation. However, the underlying molecular mechanisms remain poorly understood. Based on recent RNA sequencing experiments, DEK expression was necessary for the transcription of several metabolic enzymes involved in anabolic pathways. This identified a possible mechanism whereby DEK may drive cellular metabolism to enable cell proliferation...
2017: PloS One
https://www.readbyqxmd.com/read/28552678/detection-of-6-demethoxyubiquinone-in-coq10-deficiency-disorders-insights-into-enzyme-interactions-and-identification-of-potential-therapeutics
#15
Diran Herebian, Annette Seibt, Sander H J Smits, Gisela Bünning, Christoph Freyer, Holger Prokisch, Daniela Karall, Anna Wredenberg, Anna Wedell, Luis C López, Ertan Mayatepek, Felix Distelmaier
Coenzyme Q10 (CoQ10) is an essential cofactor of the mitochondrial oxidative phosphorylation (OXPHOS) system and its deficiency has important implications for several inherited metabolic disorders of childhood. The biosynthesis of CoQ10 is a complicated process, which involves at least 12 different enzymes. One of the metabolic intermediates that are formed during CoQ10 biosynthesis is the molecule 6-demethoxyubiquinone (6-DMQ). This CoQ precursor is processed at the level of COQ7 and COQ9. We selected this metabolite as a marker substance for metabolic analysis of cell lines with inherited genetic defects (COQ2, COQ4, COQ7 and COQ9) or siRNA knockdown in CoQ biosynthesis enzymes using ultra-performance liquid chromatography coupled to tandem mass spectrometry (UPLC-MS/MS)...
May 20, 2017: Molecular Genetics and Metabolism
https://www.readbyqxmd.com/read/28540666/evaluation-of-mitochondrial-respiratory-function-in-highly-glycolytic-glioma-cells-reveals-low-adp-phosphorylation-in-relation-to-oxidative-capacity
#16
Erika Rodrigues-Silva, Edilene S Siqueira-Santos, Juliana S Ruas, Raffaela S Ignarro, Tiago R Figueira, Fábio Rogério, Roger F Castilho
High-grade gliomas are aggressive and intensely glycolytic tumors. In the present study, we evaluated the mitochondrial respiratory function of glioma cells (T98G and U-87MG) and fresh human glioblastoma (GBM) tissue. To this end, measurements of oxygen consumption rate (OCR) were performed under various experimental conditions. The OCR of T98G and U-87MG cells was well coupled to ADP phosphorylation based on the ratio of ATP produced per oxygen consumed of ~2.5. In agreement, the basal OCR of GBM tissue was also partially associated with ADP phosphorylation...
May 24, 2017: Journal of Neuro-oncology
https://www.readbyqxmd.com/read/28537848/influence-of-endurance-training-on-skeletal-muscle-mitophagy-regulatory-proteins-in-type-2-diabetic-men
#17
Christian Brinkmann, Axel Przyklenk, Alexander Metten, Thorsten Schiffer, Wilhelm Bloch, Klara Brixius, Sebastian Gehlert
BACKGROUND: Mitophagy is a form of autophagy for the elimination of mitochondria. Mitochondrial content and function are reduced in the skeletal muscle of patients with type 2 diabetes mellitus (T2DM). Physical training has been shown to restore mitochondrial capacity in T2DM patients, but the role of mitophagy has not been examined in this context. This study analyzes the impact of a 3-month endurance training on important skeletal muscle mitophagy regulatory proteins and oxidative phosphorylation (OXPHOS) complexes in T2DM patients...
May 24, 2017: Endocrine Research
https://www.readbyqxmd.com/read/28531280/effects-of-calorie-restriction-and-fiber-type-on-glucose-uptake-and-abundance-of-electron-transport-chain-and-oxidative-phosphorylation-proteins-in-single-fibers-from-old-rats
#18
Haiyan Wang, Edward B Arias, Carmen S Yu, Anthony R P Verkerke, Gregory D Cartee
Calorie restriction (CR; reducing calorie intake by ~40% below ad libitum) can increase glucose uptake by insulin-stimulated muscle. Because skeletal muscle is comprised of multiple, heterogeneous fiber types, our primary aim was to determine in 23-26 months-old rats the effects of CR (initiated at 14 weeks-old) and fiber type on insulin-stimulated glucose uptake by single fibers of diverse fiber types. Isolated epitrochlearis muscles from AL and CR rats were incubated with [3H]-2-deoxyglucose ±insulin. Glucose uptake and fiber type were determined for single fibers dissected from the muscles...
May 22, 2017: Journals of Gerontology. Series A, Biological Sciences and Medical Sciences
https://www.readbyqxmd.com/read/28501483/reversal-of-bioenergetics-dysfunction-by-diphenyl-diselenide-is-critical-to-protection-against-the-acetaminophen-induced-acute-liver-failure
#19
Nélson R Carvalho, Cintia C Tassi, Fernando Dobraschinski, Guilherme P Amaral, Ana P Zemolin, Ronaldo M Golombieski, Cristiane L Dalla Corte, Jeferson L Franco, José L Mauriz, Javier González-Gallego, Félix A Soares
Physiopathological conditions such as acute liver failure (ALF) induced by acetaminophen (APAP) can often impair the mitochondrial bioenergetics. Diphenyl diselenide [(PhSe)2] has been shown protects against APAP-induced ALF. The present study aimed to clarify the signaling mechanism involved in the protection of bioenergetics dysfunction associated with ALF-induced by APAP overdose. Mice received APAP (600mg/kg) or (PhSe)2 (15.6mg/kg) alone, or APAP+(PhSe)2, all the solutions were administered by the intraperitoneal (i...
July 1, 2017: Life Sciences
https://www.readbyqxmd.com/read/28500267/impaired-mitochondrial-transcription-termination-disrupts-the-stromal-redox-poise-in-chlamydomonas
#20
Andreas Uhmeyer, Matteo Ballottari, Michela Cecchin, Lutz Wobbe
In photosynthetic eukaryotes, the metabolite exchange between chloroplast and mitochondria ensures efficient photosynthesis under saturating light conditions. The C. reinhardtii mutant stm6 is devoid of the mitochondrial transcription termination factor (mTERF) MOC1 and aberrantly expresses the mitochondrial genome, resulting in enhanced photosynthetic hydrogen production and diminished light tolerance. We analyzed the modulation of mitochondrial and chlororespiration during the acclimation of stm6 and the MOC1-complemented strain to excess light...
May 12, 2017: Plant Physiology
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