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https://www.readbyqxmd.com/read/29334409/climate-driven-mitochondrial-selection-a-test-in-australian-songbirds
#1
Annika Mae Lamb, Han Ming Gan, Chris Greening, Leo Joseph, Yin Peng Lee, Alejandra Morán-Ordóñez, Paul Sunnucks, Alexandra Pavlova
Diversifying selection between populations that inhabit different environments can promote lineage divergence within species and ultimately drive speciation. The mitochondrial genome (mitogenome) encodes essential proteins of the oxidative phosphorylation (OXPHOS) system and can be a strong target for climate-driven selection (i.e. associated with inhabiting different climates). We investigated whether Pleistocene climate changes drove mitochondrial selection and evolution within Australian birds. First, using phylogeographic analyses of the mitochondrial ND2 gene for 17 songbird species, we identified mitochondrial clades (mitolineages)...
January 15, 2018: Molecular Ecology
https://www.readbyqxmd.com/read/29331024/combination-therapy-of-lovastatin-and-ampk-activator-improves-mitochondrial-and-peroxisomal-functions-and-clinical-disease-in-eae-model
#2
Inderjit Singh, Devadoss J Samuvel, Seungho Choi, Nishant Saxena, Avtar K Singh, Jeseong Won
Recent studies report that loss and dysfunction of mitochondria and peroxisomes contribute to the myelin and axonal damage in multiple sclerosis (MS). In this study, we investigated the efficacy of lovastatin and AMPK activator (AICAR) combination on the loss and dysfunction of mitochondria and peroxisomes and myelin and axonal damage in the spinal cords, relative to the clinical disease symptoms, using a mouse model of experimental autoimmune encephalomyelitis (EAE, a model for MS). We observed that lovastatin and AICAR treatments individually provided partial protection of mitochondria/peroxisomes, myelin/axons, and thus partial attenuation of clinical disease in EAE mice...
January 13, 2018: Immunology
https://www.readbyqxmd.com/read/29328656/design-and-synthesis-of-novel-reactive-oxygen-species-inducers-for-the-treatment-of-pancreatic-ductal-adenocarcinoma
#3
Yuting Kuang, Mario Sechi, Salvatore Nurra, Mats Ljungman, Nouri Neamati
Altering redox homeostasis provides distinctive therapeutic opportunities for the treatment of pancreatic cancer. Quinazolinediones (QDs) are novel redox modulators that we previously showed to induce potent growth inhibition in pancreatic ductal adenocarcinoma (PDAC) cell lines. Our lead optimization campaign yielded QD325 as the most potent redox modulator candidate inducing substantial reactive oxygen species (ROS) in PDAC cells. Nascent RNA sequencing following treatments with the QD compounds revealed induction of stress responses in nucleus, endoplasmic reticulum, and mitochondria of pancreatic cancer cells...
January 12, 2018: Journal of Medicinal Chemistry
https://www.readbyqxmd.com/read/29323266/aif-loss-deregulates-hematopoiesis-and-reveals-different-adaptive-metabolic-responses-in-bone-marrow-cells-and-thymocytes
#4
Lauriane Cabon, Audrey Bertaux, Marie-Noëlle Brunelle-Navas, Ivan Nemazanyy, Laurianne Scourzic, Laure Delavallée, Laura Vela, Mathieu Baritaud, Sandrine Bouchet, Cécile Lopez, Vu Quang Van, Kevin Garbin, Danielle Chateau, Françoise Gilard, Marika Sarfati, Thomas Mercher, Olivier A Bernard, Santos A Susin
Mitochondrial metabolism is a tightly regulated process that plays a central role throughout the lifespan of hematopoietic cells. Herein, we analyze the consequences of the mitochondrial oxidative phosphorylation (OXPHOS)/metabolism disorder associated with the cell-specific hematopoietic ablation of apoptosis-inducing factor (AIF). AIF-null (AIF-/Y ) mice developed pancytopenia that was associated with hypocellular bone marrow (BM) and thymus atrophy. Although myeloid cells were relatively spared, the B-cell and erythroid lineages were altered with increased frequencies of precursor B cells, pro-erythroblasts I, and basophilic erythroblasts II...
January 11, 2018: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29317722/loss-of-the-mitochondrial-fatty-acid-%C3%AE-oxidation-protein-medium-chain-acyl-coenzyme-a-dehydrogenase-disrupts-oxidative-phosphorylation-protein-complex-stability-and-function
#5
Sze Chern Lim, Makiko Tajika, Masaru Shimura, Kirstyn T Carey, David A Stroud, Kei Murayama, Akira Ohtake, Matthew McKenzie
Medium-chain acyl-Coenzyme A dehydrogenase (MCAD) is involved in the initial step of mitochondrial fatty acid β-oxidation (FAO). Loss of function results in MCAD deficiency, a disorder that usually presents in childhood with hypoketotic hypoglycemia, vomiting and lethargy. While the disruption of mitochondrial fatty acid metabolism is the primary metabolic defect, secondary defects in mitochondrial oxidative phosphorylation (OXPHOS) may also contribute to disease pathogenesis. Therefore, we examined OXPHOS activity and stability in MCAD-deficient patient fibroblasts that have no detectable MCAD protein...
January 9, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29314548/clinical-biochemical-and-genetic-features-associated-with-vars2-related-mitochondrial-disease
#6
Francesco Bruni, Ivano Di Meo, Emanuele Bellacchio, Bryn D Webb, Robert McFarland, Zofia M A Chrzanowska-Lightowlers, Langping He, Ewa Skorupa, Isabella Moroni, Anna Ardissone, Anna Walczak, Henna Tyynismaa, Pirjo Isohanni, Hanna Mandel, Holger Prokisch, Tobias Haack, Penelope E Bonnen, Bertini Enrico, Ewa Pronicka, Daniele Ghezzi, Robert W Taylor, Daria Diodato
In recent years, an increasing number of mitochondrial disorders have been associated with mutations in mitochondrial aminoacyl-tRNA synthetases (mt-aaRSs), which are key enzymes of mitochondrial protein synthesis. Bi-allelic functional variants in VARS2, encoding the mitochondrial valyl tRNA-synthetase, were first reported in a patient with psychomotor delay and epilepsia partialis continua associated with an oxidative phosphorylation (OXPHOS) complex I defect, before being described in a patient with a neonatal form of encephalocardiomyopathy...
January 3, 2018: Human Mutation
https://www.readbyqxmd.com/read/29314417/a-nestin-cdk5-drp1-axis-regulates-neural-stem-progenitor-cell-stemness-via-a-metabolic-shift
#7
Jiancheng Wang, Yinong Huang, Jianye Cai, Qiong Ke, Jiaqi Xiao, Weijun Huang, Hongyu Li, Yuan Qiu, Yi Wang, Bin Zhang, Haoxiang Wu, Yanan Zhang, Xin Sui, Adham Sameer A Bardeesi, Andy Peng Xiang
Neural stem/progenitor cells (NSPCs) transplantation provides an alternative approach for various central nervous system (CNS) diseases treatment, while the difficulties in NSPC acquisition and expansion limit their further application. Unveiling the mechanism of NSPC stemness regulation may contribute to its further application. Nestin, generally recognized as a marker of NSPCs, plays a crucial role in the CNS development and NSPC stemness maintenance. Here, we report that Nestin loss triggers mitochondrial network remodeling and enhances oxidative phosphorylation (OXPHOS) in NSPCs treated with Nestin RNA interference (RNAi)...
January 3, 2018: Stem Cells
https://www.readbyqxmd.com/read/29306548/disrupting-the-warburg-effect-re-routes-cancer-cells-to-oxphos-offering-a-vulnerability-point-via-ferroptosis-induced-cell-death
#8
REVIEW
Maša Ždralević, Milica Vučetić, Boutaina Daher, Ibtissam Marchiq, Scott K Parks, Jacques Pouysségur
The evolution of life from extreme hypoxic environments to an oxygen-rich atmosphere has progressively selected for successful metabolic, enzymatic and bioenergetic networks through which a myriad of organisms survive the most extreme environmental conditions. From the two lethal environments anoxia/high O2, cells have developed survival strategies through expression of the transcriptional factors ATF4, HIF1 and NRF2. Cancer cells largely exploit these factors to thrive and resist therapies. In this review, we report and discuss the potential therapeutic benefit of disrupting the major Myc/Hypoxia-induced metabolic pathway, also known as fermentative glycolysis or "Warburg effect", in aggressive cancer cell lines...
December 28, 2017: Advances in Biological Regulation
https://www.readbyqxmd.com/read/29299929/proteome-of-bovine-mitochondria-and-rod-outer-segment-disks-commonalities-and-differences
#9
Maurizio Bruschi, Andrea Petretto, Federico Caicci, Martina Bartolucci, Daniela Calzia, Laura Santucci, Lucia Manni, Luca A Ramenghi, Gian Marco Ghiggeri, Carlo E Traverso, Giovanni Candiano, Isabella Panfoli
The retinal rod outer segment (OS) is a stack of disks surrounded by the plasma membrane, housing proteins related to phototransduction, as well as mitochondrial proteins involved in oxidative phosphorylation (OxPhos). This prompted us to compare the proteome of bovine OS disks and mitochondria, to assess the significant top gene signatures of each sample. The two proteomes, obtained by LTQ-Orbitrap Velos mass spectrometry, were compared by statistical analyses. 4139 proteins were identified, 2045 of which overlapping in the two sets...
January 4, 2018: Journal of Proteome Research
https://www.readbyqxmd.com/read/29298418/neuronal-pas-domain-protein-4-suppression-of-oxygen-sensing-optimizes-metabolism-during-excitation-of-neuroendocrine-cells
#10
Paul V Sabatini, Thilo Speckmann, Cuilan Nian, Maria M Glavas, Chi Kin Wong, Ji Soo Yoon, Tatsuya Kin, A M James Shapiro, William T Gibson, C Bruce Verchere, Francis C Lynn
Depolarization of neuroendocrine cells results in calcium influx, which induces vesicle exocytosis and alters gene expression. These processes, along with the restoration of resting membrane potential, are energy intensive. We hypothesized that cellular mechanisms exist to maximize energy production during excitation. Here, we demonstrate that NPAS4, an immediate early basic helix-loop-helix (bHLH)-PAS transcription factor, acts to maximize energy production by suppressing hypoxia-inducible factor 1α (HIF1α)...
January 2, 2018: Cell Reports
https://www.readbyqxmd.com/read/29296613/mglur2-3-activation-of-the-sirt1-axis-preserves-mitochondrial-function-in-diabetic-neuropathy
#11
Krish Chandrasekaran, Anjaneyulu Muragundla, Tyler G Demarest, Joungil Choi, Avinash R Sagi, Neda Najimi, Pranith Kumar, Anmol Singh, Cheng-Ying Ho, Gary Fiskum, Lauren G Koch, Steven L Britton, James W Russell
Objectives: There is a critical need to develop effective treatments for diabetic neuropathy. This study determined if a selective mGluR2/3 receptor agonist prevented or treated experimental diabetic peripheral neuropathy (DPN) through glutamate recycling and improved mitochondrial function. Methods: Adult male streptozotocin treated Sprague-Dawley rats with features of type 1 diabetes mellitus (T1DM) or Low Capacity Running (LCR) rats with insulin resistance or glucose intolerance were treated with 3 or 10 mg/kg/day LY379268...
December 2017: Annals of Clinical and Translational Neurology
https://www.readbyqxmd.com/read/29285300/renal-oncocytoma-characterized-by-the-defective-complex-i-of-the-respiratory-chain-boosts-the-synthesis-of-the-ros-scavenger-glutathione
#12
Gerrit Kürschner, Qingzhou Zhang, Rosanna Clima, Yi Xiao, Jonas Felix Busch, Ergin Kilic, Klaus Jung, Nikolaus Berndt, Sascha Bulik, Hermann-Georg Holzhütter, Giuseppe Gasparre, Marcella Attimonelli, Mohan Babu, David Meierhofer
Renal oncocytomas are rare benign tumors of the kidney and characterized by a deficient complex I (CI) enzyme activity of the oxidative phosphorylation (OXPHOS) system caused by mitochondrial DNA (mtDNA) mutations. Yet, little is known about the underlying molecular mechanisms and alterations of metabolic pathways in this tumor. We compared renal oncocytomas with adjacent matched normal kidney tissues on a global scale by multi-omics approaches, including whole exome sequencing (WES), proteomics, metabolomics, and metabolic pathway simulation...
December 1, 2017: Oncotarget
https://www.readbyqxmd.com/read/29281973/polymorphic-duplicate-genes-and-persistent-non-coding-sequences-reveal-heterogeneous-patterns-of-mitochondrial-dna-loss-in-salamanders
#13
Rebecca A Chong, Rachel Lockridge Mueller
BACKGROUND: Mitochondria are the site of the citric acid cycle and oxidative phosphorylation (OXPHOS). In metazoans, the mitochondrial genome is a small, circular molecule averaging 16.5 kb in length. Despite evolutionarily conserved gene content, metazoan mitochondrial genomes show a diversity of gene orders most commonly explained by the duplication-random loss (DRL) model. In the DRL model, (1) a sequence of genes is duplicated in tandem, (2) one paralog sustains a loss-of-function mutation, resulting in selection to retain the other copy, and (3) the non-functional paralog is eventually deleted from the genome...
December 28, 2017: BMC Genomics
https://www.readbyqxmd.com/read/29281964/the-molecular-evolutionary-dynamics-of-oxidative-phosphorylation-oxphos-genes-in-hymenoptera
#14
Yiyuan Li, Rui Zhang, Shanlin Liu, Alexander Donath, Ralph S Peters, Jessica Ware, Bernhard Misof, Oliver Niehuis, Michael E Pfrender, Xin Zhou
BACKGROUND: The primary energy-producing pathway in eukaryotic cells, the oxidative phosphorylation (OXPHOS) system, comprises proteins encoded by both mitochondrial and nuclear genes. To maintain the function of the OXPHOS system, the pattern of substitutions in mitochondrial and nuclear genes may not be completely independent. It has been suggested that slightly deleterious substitutions in mitochondrial genes are compensated by substitutions in the interacting nuclear genes due to positive selection...
December 28, 2017: BMC Evolutionary Biology
https://www.readbyqxmd.com/read/29281123/mitochondrial-dna-damage-and-reactive-oxygen-species-in-neurodegenerative-disease
#15
REVIEW
Nadee Nissanka, Carlos T Moraes
Mitochondria are essential organelles within the cell where most ATP is produced through oxidative phosphorylation (OXPHOS). A subset of the genes needed for this process are encoded by the mitochondrial DNA (mtDNA). One consequence of OXPHOS is the production of mitochondrial reactive oxygen species (ROS), whose role in mediating cellular damage, particularly in damaging mtDNA during aging, has been controversial. There are subsets of neurons that appear to be more sensitive to ROS-induced damage, and mitochondrial dysfunction has been associated with several neurodegenerative disorders...
December 27, 2017: FEBS Letters
https://www.readbyqxmd.com/read/29248374/multi-omics-reveal-specific-targets-of-the-rna-binding-protein-puf3p-and-its-orchestration-of-mitochondrial-biogenesis
#16
Christopher P Lapointe, Jonathan A Stefely, Adam Jochem, Paul D Hutchins, Gary M Wilson, Nicholas W Kwiecien, Joshua J Coon, Marvin Wickens, David J Pagliarini
Coenzyme Q (CoQ) is a redox-active lipid required for mitochondrial oxidative phosphorylation (OxPhos). How CoQ biosynthesis is coordinated with the biogenesis of OxPhos protein complexes is unclear. Here, we show that the Saccharomyces cerevisiae RNA-binding protein (RBP) Puf3p regulates CoQ biosynthesis. To establish the mechanism for this regulation, we employed a multi-omic strategy to identify mRNAs that not only bind Puf3p but also are regulated by Puf3p in vivo. The CoQ biosynthesis enzyme Coq5p is a critical Puf3p target: Puf3p regulates the abundance of Coq5p and prevents its detrimental hyperaccumulation, thereby enabling efficient CoQ production...
December 12, 2017: Cell Systems
https://www.readbyqxmd.com/read/29248133/hodgkin-lymphoma-a-complex-metabolic-ecosystem-with-glycolytic-reprogramming-of-the-tumor-microenvironment
#17
Lekha Mikkilineni, Diana Whitaker-Menezes, Marina Domingo-Vidal, John Sprandio, Paola Avena, Paolo Cotzia, Alina Dulau-Florea, Jerald Gong, Guldeep Uppal, Tingting Zhan, Benjamin Leiby, Zhao Lin, Barbara Pro, Federica Sotgia, Michael P Lisanti, Ubaldo Martinez-Outschoorn
BACKGROUND: Twenty percent of patients with classical Hodgkin Lymphoma (cHL) have aggressive disease defined as relapsed or refractory disease to initial therapy. At present we cannot identify these patients pre-treatment. The microenvironment is very important in cHL because non-cancer cells constitute the majority of the cells in these tumors. Non-cancer intra-tumoral cells, such as tumor-associated macrophages (TAMs) have been shown to promote tumor growth in cHL via crosstalk with the cancer cells...
June 2017: Seminars in Oncology
https://www.readbyqxmd.com/read/29248132/mitochondrial-and-glycolytic-metabolic-compartmentalization-in-diffuse-large-b-cell-lymphoma
#18
Mahasweta Gooptu, Diana Whitaker-Menezes, John Sprandio, Marina Domingo-Vidal, Zhao Lin, Guldeep Uppal, Jerald Gong, Roberto Fratamico, Benjamin Leiby, Alina Dulau-Florea, Jaime Caro, Ubaldo Martinez-Outschoorn
Metabolic heterogeneity between neoplastic cells and surrounding stroma has been described in several epithelial malignancies; however, the metabolic phenotypes of neoplastic lymphocytes and neighboring stroma in diffuse large B-cell lymphoma (DLBCL) is unknown. We investigated the metabolic phenotypes of human DLBCL tumors by using immunohistochemical markers of glycolytic and mitochondrial oxidative phosphorylation (OXPHOS) metabolism. The lactate importer MCT4 is a marker of glycolysis, whereas the lactate importer MCT1 and TOMM20 are markers of OXPHOS metabolism...
June 2017: Seminars in Oncology
https://www.readbyqxmd.com/read/29235020/do-gstm1-and-gstt1-polymorphisms-influence-the-risk-of-developing-mitochondrial-diseases-in-a-tunisian-population
#19
Raouia Ghorbel, Ghada Ben Salah, Rania Ghorbel, Afif Ben Mahmoud, Imen Chamkha, Emna Mkaouar-Rebai, Leila Ammar-Keskes, Faiza Fakhfakh
Mitochondria play an essential role to supply the cell with metabolic energy in the form of adenosine triphosphate (ATP) through oxidative phosphorylation (OXPHOS). As a consequence, they are also the primary source of cellular reactive oxygen species (ROS) which can cause oxidative damage of individual respiratory chain complexes. Indeed, affected OXPHOS subunits result in decreases in ATP production and increases in ROS formation which generate oxidative phosphorylation deficiency leading to mitochondrial dysfunctions...
December 12, 2017: Environmental Science and Pollution Research International
https://www.readbyqxmd.com/read/29218518/evaluating-the-efficacy-of-glut-inhibitors-using-a-seahorse-extracellular-flux-analyzer
#20
Changyong Wei, Monique Heitmeier, Paul W Hruz, Mala Shanmugam
Glucose is metabolized through anaerobic glycolysis and aerobic oxidative phosphorylation (OXPHOS). Perturbing glucose uptake and its subsequent metabolism can alter both glycolytic and OXPHOS pathways and consequently lactate and/or oxygen consumption. Production and secretion of lactate, as a consequence of glycolysis, leads to acidification of the extracellular medium. Molecular oxygen is the final electron acceptor in the electron transport chain, facilitating oxidative phosphorylation of ADP to ATP. The alterations in extracellular acidification and/or oxygen consumption can thus be used as indirect readouts of glucose metabolism and assessing the impact of inhibiting glucose transport through specific glucose transporters (GLUTs)...
2018: Methods in Molecular Biology
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