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https://www.readbyqxmd.com/read/29054837/altered-metabolic-landscape-in-idh-mutant-gliomas%C3%A2-affects-phospholipid-energy-and-oxidative-stress-pathways
#1
Fred Fack, Saverio Tardito, Guillaume Hochart, Anais Oudin, Liang Zheng, Sabrina Fritah, Anna Golebiewska, Petr V Nazarov, Amandine Bernard, Ann-Christin Hau, Olivier Keunen, William Leenders, Morten Lund-Johansen, Jonathan Stauber, Eyal Gottlieb, Rolf Bjerkvig, Simone P Niclou
Heterozygous mutations in NADP-dependent isocitrate dehydrogenases (IDH) define the large majority of diffuse gliomas and are associated with hypermethylation of DNA and chromatin. The metabolic dysregulations imposed by these mutations, whether dependent or not on the oncometabolite D-2-hydroxyglutarate (D2HG), are less well understood. Here, we applied mass spectrometry imaging on intracranial patient-derived xenografts of IDH-mutant versus IDH wild-type glioma to profile the distribution of metabolites at high anatomical resolution in situ This approach was complemented by in vivo tracing of labeled nutrients followed by liquid chromatography-mass spectrometry (LC-MS) analysis...
October 20, 2017: EMBO Molecular Medicine
https://www.readbyqxmd.com/read/29054072/cysteine-perthiosulfenic-acid-cys-ssoh-a-novel-intermediate-in-thiol-based-redox-signaling
#2
David E Heppner, Milena Hristova, Tomoaki Ida, Ana Mijuskovic, Christopher M Dustin, Virág Bogdándi, Jon M Fukuto, Tobias P Dick, Péter Nagy, Jianing Li, Takaaki Akaike, Albert van der Vliet
The reversible oxidation of protein cysteine residues (Cys-SH) is a key reaction in cellular redox signaling involving initial formation of sulfenic acids (Cys-SOH), which are commonly detected using selective dimedone-based probes. Here, we report that significant portions of dimedone-tagged proteins are susceptible to cleavage by DTT reflecting the presence of perthiosulfenic acid species (Cys-SSOH) due to similar oxidation of hydropersulfides (Cys-SSH), since Cys-S-dimedone adducts are stable toward DTT...
October 9, 2017: Redox Biology
https://www.readbyqxmd.com/read/29053963/hydrilla-verticillata-employs-two-different-ways-to-affect-dna-methylation-under-excess-copper-stress
#3
Danlu Shi, Kai Zhuang, Yan Xia, Changhua Zhu, Chen Chen, Zhubing Hu, Zhenguo Shen
Because of the accumulation of heavy metals, Hydrilla verticillata (L.f.) Royle, a rooted submerged perennial aquatic herb, is being developed as a potential tool to clean the aquatic ecosystem polluted by heavy metals. However, its physiological responses for heavy metal remain to be elucidated. Here, through employing proteomics approach, we found that excess Cu significantly induced the expressions of four DNA methylation related proteins in H. verticillata, which were the homologues of two domains rearranged methyltransferases (DRM), a methyltransferases chromomethylase (CMT) and a histone H3 lysine-9 specific SUVH6-like (SUVH6)...
October 14, 2017: Aquatic Toxicology
https://www.readbyqxmd.com/read/29051509/the-transcriptional-regulator-ntrc-controls-glucose-6-phosphate-dehydrogenase-expression-and-polyhydroxybutyrate-synthesis-through-nadph-availability-in-herbaspirillum-seropedicae
#4
Euclides Nenga Manuel Sacomboio, Edson Yu Sin Kim, Henrique Leonardo Ruchaud Correa, Paloma Bonato, Fabio de Oliveira Pedrosa, Emanuel Maltempi de Souza, Leda Satie Chubatsu, Marcelo Müller-Santos
The NTR system is the major regulator of nitrogen metabolism in Bacteria. Despite its broad and well-known role in the assimilation, biosynthesis and recycling of nitrogenous molecules, little is known about its role in carbon metabolism. In this work, we present a new facet of the NTR system in the control of NADPH concentration and the biosynthesis of molecules dependent on reduced coenzyme in Herbaspirillum seropedicae SmR1. We demonstrated that a ntrC mutant strain accumulated high levels of polyhydroxybutyrate (PHB), reaching levels up to 2-fold higher than the parental strain...
October 19, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29051480/nox4-functions-as-a-mitochondrial-energetic-sensor-coupling-cancer-metabolic-reprogramming-to-drug-resistance
#5
Karthigayan Shanmugasundaram, Bijaya K Nayak, William E Friedrichs, Dharam Kaushik, Ronald Rodriguez, Karen Block
The molecular mechanisms that couple glycolysis to cancer drug resistance remain unclear. Here we identify an ATP-binding motif within the NADPH oxidase isoform, NOX4, and show that ATP directly binds and negatively regulates NOX4 activity. We find that NOX4 localizes to the inner mitochondria membrane and that subcellular redistribution of ATP levels from the mitochondria act as an allosteric switch to activate NOX4. We provide evidence that NOX4-derived reactive oxygen species (ROS) inhibits P300/CBP-associated factor (PCAF)-dependent acetylation and lysosomal degradation of the pyruvate kinase-M2 isoform (PKM2)...
October 19, 2017: Nature Communications
https://www.readbyqxmd.com/read/29050764/pharmacokinetic-studies-of-a-three-component-complex-that-repurposes-the-front-line-antibiotic-isoniazid-against-mycobacterium-tuberculosis
#6
Thomas J Manning, Kyle Wilkerson, Taylor Holder, Andrew Carson Bartley, Chelsea Jackson, Sydney Plummer, Dennis Phillips, Logan Krajewski, Greg Wylie
The frontline tuberculosis (Tb) antibiotic isoniazid has been repurposed using a three component complex aimed at increasing the delivery efficiency and adding new avenues to its mechanism of action. This study focuses on pharmacokinetic studies of the isoniazid-sucrose-copper (II)-PEG-3350 complex. The assays include the Plasma Protein Binding Assay (85.8%), Caco-2 Permeability Assay (B→APapp, 0.13 × 10(-6) cm/s), Cytochrome P450 Inhibition Assay (i.e. CYP2B6, IC50 = 7.26 μM), In vitro microsomal Stability Assay (t1/2 NADPH-Dependent > 240 min), and HepG2 Cytotoxicity (no toxicity)...
December 2017: Tuberculosis
https://www.readbyqxmd.com/read/29050522/metabolism-of-megestrol-acetate-in-vitro-and-the-role-of-oxidative-metabolites
#7
Larry House, Michael Seminerio, Snezana Mirkov, Jacqueline Ramirez, Maxwell Skor, Joseph Sachleben, Masis Isikbay, Hari Singhal, Geoffrey Greene, Donald Vander Griend, Suzanne Conzen, Mark J Ratain
There is limited knowledge regarding the metabolism of megestrol acetate (MA), as it was approved by FDA in 1971, prior to the availability of modern tools for identifying specific drug-metabolizing enzymes. We determined the cytochrome P450s (P450s) and UDP-glucuronosyltransferases (UGTs) that metabolize MA, identified oxidative metabolites, and determined pharmacologic activity at the progesterone, androgen and glucocorticoid receptors (PR, AR, and GR, respectively). Oxidative metabolites were produced using human liver microsomes (HLMs), and isolated for mass spectral (MS) and nuclear magnetic resonance (NMR) analyses...
October 20, 2017: Xenobiotica; the Fate of Foreign Compounds in Biological Systems
https://www.readbyqxmd.com/read/29050006/recent-insights-into-the-biological-functions-of-sestrins-in-health-and-disease
#8
Menglong Wang, Yao Xu, Jianfang Liu, Jing Ye, Wenhui Yuan, Huimin Jiang, Zhen Wang, Hong Jiang, Jun Wan
Sestrins (Sesns) have been identified as a family of highly conserved stress-inducible proteins that are strongly up-regulated by various stresses, including DNA damage, oxidative stress, and hypoxia. The Sesns play protective roles in most physiological and pathological conditions mainly through the regulation of oxidative stress, inflammation, autophagy, endoplasmic reticulum stress, and metabolic homeostasis. In this review, we discussed the possible regulators of Sesns expression, such as p53, forkhead box O, nuclear factor erythroid 2 like 2 (Nrf2), NH (2)-terminal kinase (JNK)/c-Jun pathway and hypoxia-inducible factor-1α (Hif-1α), and the downstream pathways regulated by the Sesns including AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) signaling, mitogen-activated protein kinases (MAPKs) signaling, Nrf2 signaling, NADPH oxidase signaling and transforming growth factor β (TGF-β) signaling in heart diseases, lung diseases, gastrointestinal tract diseases, liver and metabolism diseases, neurological diseases, kidney diseases and immunological diseases...
October 19, 2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/29049376/antioxidants-and-nox1-nox4-inhibition-blocks-tgf%C3%AE-1-induced-ccn2-and-%C3%AE-sma-expression-in-dermal-and-gingival-fibroblasts
#9
Hannah Murphy-Marshman, Katherine Quensel, Xu Shi-Wen, Rebecca Barnfield, Jacalyn Kelly, Alex Peidl, Richard J Stratton, Andrew Leask
TGFbeta induces fibrogenic responses in fibroblasts. Reactive oxygen species (ROS)/nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) may contribute to fibrogenic responses. Here, we examine if the antioxidant N-acetylcysteine (NAC), the NOX inhibitor diphenyleneiodonium (DPI) and the selective NOX1/NOX4 inhibitor GKT-137831 impairs the ability of TGFbeta to induce profibrotic gene expression in human gingival (HGF) and dermal (HDF) fibroblasts. We also assess if GKT-137831 can block the persistent fibrotic phenotype of lesional scleroderma (SSc) fibroblasts...
2017: PloS One
https://www.readbyqxmd.com/read/29048637/leptin-induces-ros-via-nox5-in-healthy-and-neoplastic-mammary-epithelial-cells
#10
Sinda Mahbouli, Audrey Der Vartanian, Sophie Ortega, Stéphanie Rougé, Marie-Paule Vasson, Adrien Rossary
NADPH oxidase (NOX) complexes (a family of seven isoforms) drive cellular ROS production in patho-logical processes such as cancer. NOX-driven ROS production is involved in cell mechanisms from signalling to oxidative stress. Leptin, an adipokine overexpressed in obese patients, has been investigated in studies on breast carcinogenesis, but its effects on oxidative stress remain largely unexplored, especially in breast cancer. The study used three human mammary epithelial cell models presenting different neoplastic status (healthy primary HMECs, neoplastic MCF-7 cells and neoplastic MDA-MB-231 cells) to determine the effects of leptin on short-term ROS production and to characterize the enzymes involved...
September 27, 2017: Oncology Reports
https://www.readbyqxmd.com/read/29047097/from-physiological-redox-signalling-to-oxidant-stress
#11
Jeremy P T Ward
Oxidant stress is strongly associated with cardiovascular disease, including pulmonary hypertension, but antioxidant therapies have so far proven ineffective. This is partly due to a lack of understanding of the key role played by reactive oxygen species (ROS) in physiological cell signalling, and partly to the complex interrelationships between generators of ROS (e.g. mitochondria and NADPH oxidases, NOX), cellular antioxidant systems and indeed Ca(2+) signalling. At physiological levels ROS reversibly affect the function of numerous enzymes and transcription factors, most often via oxidation of specific protein thiols...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/29047094/endothelial-cell-reactive-oxygen-species-and-ca-2-signaling-in-pulmonary-hypertension
#12
Karthik Suresh, Larissa A Shimoda
Pulmonary hypertension (PH) refers to a disorder characterized by elevated pulmonary arterial pressure, leading to right ventricular overload and eventually right ventricular failure, which results in high morbidity and mortality. PH is associated with heterogeneous etiologies and distinct molecular mechanisms, including abnormal migration and proliferation of endothelial and smooth muscle cells. Although the exact details are not fully elucidated, reactive oxygen species (ROS) have been shown to play a key role in promoting abnormal function in pulmonary arterial smooth muscle and endothelial cells in PH...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/29047093/cross-talk-between-mitochondrial-reactive-oxygen-species-and-sarcoplasmic-reticulum-calcium-in-pulmonary-arterial-smooth-muscle-cells
#13
Tengyao Song, Yun-Min Zheng, Yong-Xiao Wang
Hypoxic pulmonary vasoconstriction (HPV) occurs during both fetal and postnatal development and plays a critical role in matching regional alveolar perfusion with ventilation in humans and animals. HPV also contributes significantly to the development of pulmonary hypertension. Although the molecular mechanisms of HPV and pulmonary hypertension remain incompletely understood, increasing evidence demonstrates that hypoxia induces an elevated intracellular reactive oxygen species concentration ([ROS]i) in pulmonary artery smooth muscle cells (PASMCs)...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/29047089/redox-mechanisms-influencing-cgmp-signaling-in-pulmonary-vascular-physiology-and-pathophysiology
#14
Dhara Patel, Anand Lakhkar, Michael S Wolin
The soluble form of guanylate cyclase (sGC) and cGMP signaling are major regulators of pulmonary vasodilation and vascular remodeling that protect the pulmonary circulation from hypertension development. Nitric oxide, reactive oxygen species, thiol and heme redox, and heme biosynthesis control mechanisms regulating the production of cGMP by sGC. In addition, a cGMP-independent mechanism regulates protein kinase G through thiol oxidation in manner controlled by peroxide metabolism and NADPH redox. Multiple aspects of these regulatory processes contribute to physiological and pathophysiological regulation of the pulmonary circulation, and create potentially novel therapeutic targets for the treatment of pulmonary vascular disease...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/29047088/lung-ischaemia-reperfusion-injury-the-role-of-reactive-oxygen-species
#15
Oleg Pak, Akylbek Sydykov, Djuro Kosanovic, Ralph T Schermuly, Alexander Dietrich, Katrin Schröder, Ralf P Brandes, Thomas Gudermann, Natascha Sommer, Norbert Weissmann
Lung ischaemia-reperfusion injury (LIRI) occurs in many lung diseases and during surgical procedures such as lung transplantation. The re-establishment of blood flow and oxygen delivery into the previously ischaemic lung exacerbates the ischaemic injury and leads to increased microvascular permeability and pulmonary vascular resistance as well as to vigorous activation of the immune response. These events initiate the irreversible damage of the lung with subsequent oedema formation that can result in systemic hypoxaemia and multi-organ failure...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/29047081/redox-regulation-of-the-superoxide-dismutases-sod3-and-sod2-in-the-pulmonary-circulation
#16
Daniel Hernandez-Saavedra, Kalin Swain, Rubin Tuder, Steen V Petersen, Eva Nozik-Grayck
When evaluating the role of redox-regulating signaling in pulmonary vascular diseases, it is intriguing to consider the modulation of key antioxidant enzymes like superoxide dismutase (SOD) because SOD isoforms are regulated by redox reactions, and, in turn, modulate downstream redox sensitive processes. The emerging field of redox biology is built upon understanding the regulation and consequences of tightly controlled and specific reduction-oxidation reactions that are critical for diverse cellular processes including cell signaling...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/29047080/pentose-shunt-glucose-6-phosphate-dehydrogenase-nadph-redox-and-stem-cells-in-pulmonary-hypertension
#17
Ryota Hashimoto, Sachin Gupte
Redox signaling plays a critical role in the pathophysiology of cardiovascular diseases. The pentose phosphate pathway is a major source of NADPH redox in the cell. The activities of glucose-6-phosphate dehydrogenase (the rate-limiting enzyme in the pentose shunt) and glucose flux through the shunt pathway is increased in various lung cells including, the stem cells, in pulmonary hypertension. This chapter discusses the importance of the shunt pathway and glucose-6-phosphate dehydrogenase in the pathogenesis of pulmonary artery remodeling and occlusive lesion formation within the hypertensive lungs...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/29047077/adventitial-fibroblast-nox4-expression-and-ros-signaling-in-pulmonary-arterial-hypertension
#18
Scott A Barman, David Fulton
Pulmonary arterial hypertension (PAH) is a progressive disease arising from remodeling and narrowing of pulmonary arteries (PA) resulting in high pulmonary arterial blood pressure and ultimately right ventricular failure. Elevated production of reactive oxygen species (ROS) by NADPH oxidase 4 (Nox4), a constitutively active enzyme, has been associated with oxygen sensing, vasomotor control, cellular proliferation, differentiation, migration, apoptosis, senescence, fibrosis, and angiogenesis. Further, elevated expression of Nox4 has been reported in a number of cardiovascular diseases, including atherosclerosis, hypertension, cardiac failure, ischemic stroke, and PAH...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/29046349/differential-regulation-of-the-rac1-gtpase-activating-protein-gap-bcr-during-oxygen-glucose-deprivation-in-hippocampal-and-cortical-neurons
#19
Katharine R Smith, Dipen Rajgor, Jonathan G Hanley
Brain ischemia causes oxygen and glucose deprivation (OGD) in neurons, triggering a cascade of events leading to synaptic accumulation of glutamate. Excessive activation of glutamate receptors causes excitotoxicity and delayed cell death in vulnerable neurons. Following global cerebral ischemia, hippocampal CA1 pyramidal neurons are more vulnerable to injury than their cortical counterparts, but the mechanisms that underlie this difference are unclear. Signalling via Rho-family small GTPases, their upstream Guanine nucleotide Exchange Factors (GEFs) and GTPase Activating Proteins (GAPs) is differentially dysregulated in response to OGD/ischemia in hippocampal and cortical neurons...
October 18, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/29046340/nnt-is-a-key-regulator-of-adrenal-redox-homeostasis-and-steroidogenesis-in-male-mice
#20
Eirini Meimaridou, Michelle Goldsworthy, Vasileios Chortis, Ersi Fragouli, Paul A Foster, Wiebke Arlt, Roger Cox, Louise A Metherell
Nicotinamide nucleotide transhydrogenase, NNT, is a ubiquitous protein of the inner mitochondrial membrane with a key role in mitochondrial redox balance. NNT produces high concentrations of NADPH for detoxification of reactive oxygen species by glutathione and thioredoxin pathways. In humans, NNT dysfunction leads to an adrenal specific disorder, glucocorticoid deficiency. Certain sub-strains of C57BL/6 mice contain a spontaneously occurring inactivating Nnt mutation and display glucocorticoid deficiency along with glucose intolerance and reduced insulin secretion...
October 18, 2017: Journal of Endocrinology
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