Elucidating the role of copper in CHO cell energy metabolism using13C metabolic flux analysis

2015 ◽  
Vol 31 (5) ◽  
pp. 1179-1186 ◽  
Author(s):  
Shilpa Nargund ◽  
Jinshu Qiu ◽  
Chetan T. Goudar
Keyword(s):  
Energy Metabolism ◽  
Metabolic Flux Analysis ◽  
Metabolic Flux ◽  
Flux Analysis ◽  
Cho Cell ◽  
Cell Energy ◽  
Cell Energy Metabolism

scholarly journals Metabolic flux analysis during galactose and lactate co-consumption reveals enhanced energy metabolism in continuous CHO cell cultures

2019 ◽  
Vol 205 ◽  
pp. 201-211 ◽  
Author(s):  
Mauro Torres ◽  
Julio Berrios ◽  
Yandi Rigual ◽  
Yesenia Latorre ◽  
Mauricio Vergara ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Cell Cultures ◽  
Metabolic Flux Analysis ◽  
Metabolic Flux ◽  
Flux Analysis ◽  
Cho Cell

Metabolic flux analysis of CHO cell metabolism in the late non-growth phase

2010 ◽  
Vol 108 (1) ◽  
pp. 82-92 ◽  
Author(s):  
Neelanjan Sengupta ◽  
Steven T. Rose ◽  
John A. Morgan
Keyword(s):  
Growth Phase ◽  
Metabolic Flux Analysis ◽  
Metabolic Flux ◽  
Cell Metabolism ◽  
Flux Analysis ◽  
Cho Cell

scholarly journals The Role of Pool Size Measurements in Improving Flux Estimations in Non-Stationary Metabolic Flux Analysis

2019 ◽  
Vol 116 (3) ◽  
pp. 132a
Author(s):  
Anna Sher ◽  
Daniel Fridman ◽  
Jamey Young ◽  
Cynthia J. Musante
Keyword(s):  
Metabolic Flux Analysis ◽  
Metabolic Flux ◽  
Pool Size ◽  
Flux Analysis

scholarly journals AB0052 ROLE OF TRAINED IMMUNITY AND IMMUNOMETABOLISM IN THE PATHOGENESIS OF ERDHEIM-CHESTER DISEASE

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1328.2-1328
Author(s):  
R. Biavasco ◽  
R. Molteni ◽  
D. Stefanoni ◽  
M. Ferrarini ◽  
E. Ferrero ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Inflammatory Cytokines ◽  
Mapk Pathway ◽  
Inflammatory Activation ◽  
Cell Energy ◽  
Erdheim Chester ◽  
Chester Disease ◽  
Pro Inflammatory Cytokines ◽  
Cell Energy Metabolism

Background:Erdheim-Chester disease (ECD) is a chronic inflammatory disease characterized by infiltration of bone and other tissues by foamy macrophages. These cells exhibit activating mutations along the MAPK pathway, most commonly BRAFV600E, and increased production of pro-inflammatory cytokines. Although this dual neoplastic-inflammatory nature of ECD has long fascinated scientists, the mechanistic link between these two features remains elusive. We hypothesized that Trained Immunity (TI), a pro-inflammatory cell program physiologically elicited in monocytes/macrophages upon activation of the MAPK pathway, might represent the missing link between oncogenic transformation and pro-inflammatory activation in ECD.Objectives:In this study, we aimed at determining the role of TI in the pathogenesis of ECD, and to evaluate the therapeutic potential of targeting this mechanism for the treatment of inflammation.Methods:We developed innovative models to study ECD pathogenesisin vitro(based on lentiviral transduction and ectopic expression of BRAFV600E in primary human monocytes), as well asex vivo(3D culture of ECD tissue biopsies in bioreactor). Functional and mechanistic features of TI, including typical changes in cell energy metabolism and epigenetics, were investigated by assessing I) cytokine and lactate production; II) mitochondrial respiration with Seahorse flux analyzer; III) glucose, glutamine and cholesterol metabolism with unbiased and targeted metabolomics analyses; IV) epigenetic changes with ChIP PCR; V) transcriptome changes with RNA sequencing.Results:Activation of the MAPK pathway induced by BRAFV600E in macrophages induces changes in the epigenetic and gene expression landscape, cell energy metabolism, and cytokine production characteristic of TI. In particular, changes in cell energy metabolism of macrophages are characterized by increased glycolysis, glutamine metabolism, and cholesterol synthesis. This metabolic rewiring is needed to sustain rampant, constitutive production of pro-inflammatory cytokines.Conclusion:A role emerges for TI in the pathogenesis and pro-inflammatory activation of ECD. However, maladaptive activation of this mechanism is likely common to the pathogenesis of other inflammatory and rheumatologic diseases. Since drugs targeting TI programs are already entering the clinical arena, the identification of this mechanism in the pathogenesis of inflammatory and rheumatologic conditions may promptly translate into novel, effective treatment options for affected patients.Disclosure of Interests:Riccardo Biavasco Employee of: Bluebird, Raffaella Molteni: None declared, Davide Stefanoni: None declared, Marina Ferrarini: None declared, Elisabetta Ferrero: None declared, Simone Cenci: None declared, Simone Cardaci: None declared, Alessandra Boletta: None declared, Laura Cassina: None declared, Gianfranco Di Stefano: None declared, Jorge Dominguez Andres: None declared, Claudio Doglioni: None declared, Travis Nemkov: None declared, Ivan Merelli: None declared, Angelo D’Alessandro: None declared, Eugenio Montini: None declared, Mihai Netea: None declared, Lorenzo Dagna: None declared, Giulio Cavalli Consultant of: SOBI, Pfizer, Sanofi, Novartis, Paid instructor for: SOBI, Novartis, Speakers bureau: SOBI, Novartis

scholarly journals Dynamic metabolic flux analysis using B-splines to study the effects of temperature shift on CHO cell metabolism

2015 ◽  
Vol 2 ◽  
pp. 46-57 ◽  
Author(s):  
Verónica S. Martínez ◽  
Maria Buchsteiner ◽  
Peter Gray ◽  
Lars K. Nielsen ◽  
Lake-Ee Quek
Keyword(s):  
Metabolic Flux Analysis ◽  
Metabolic Flux ◽  
Cell Metabolism ◽  
Temperature Shift ◽  
Flux Analysis ◽  
Cho Cell ◽  
B Splines ◽  
Effects Of Temperature

Towards dynamic metabolic flux analysis in CHO cell cultures

2011 ◽  
Vol 7 (1) ◽  
pp. 61-74 ◽  
Author(s):  
Woo Suk Ahn ◽  
Maciek R. Antoniewicz
Keyword(s):  
Cell Cultures ◽  
Metabolic Flux Analysis ◽  
Metabolic Flux ◽  
Flux Analysis ◽  
Cho Cell

scholarly journals Metabolic flux analysis of wild-type Escherichia coli and mutants deficient in pyruvate-dissimilating enzymes during the fermentative metabolism of glucuronate

Microbiology ◽  
2010 ◽  
Vol 156 (6) ◽  
pp. 1860-1872 ◽  
Author(s):  
Abhishek Murarka ◽  
James M. Clomburg ◽  
Ramon Gonzalez
Keyword(s):  
Escherichia Coli ◽  
Metabolic Flux Analysis ◽  
Metabolic Flux ◽  
Reducing Power ◽  
Building Blocks ◽  
Exponential Phase ◽  
Flux Analysis ◽  
Wild Type ◽  
Fermentative Metabolism

The fermentative metabolism of d-glucuronic acid (glucuronate) in Escherichia coli was investigated with emphasis on the dissimilation of pyruvate via pyruvate formate-lyase (PFL) and pyruvate dehydrogenase (PDH). In silico and in vivo metabolic flux analysis (MFA) revealed that PFL and PDH share the dissimilation of pyruvate in wild-type MG1655. Surprisingly, it was found that PDH supports fermentative growth on glucuronate in the absence of PFL. The PDH-deficient strain (Pdh−) exhibited a slower transition into the exponential phase and a decrease in specific rates of growth and glucuronate utilization. Moreover, a significant redistribution of metabolic fluxes was found in PDH- and PFL-deficient strains. Since no role had been proposed for PDH in the fermentative metabolism of E. coli, the metabolic differences between MG1655 and Pdh− were further investigated. An increase in the oxidative pentose phosphate pathway (ox-PPP) flux was observed in response to PDH deficiency. A comparison of the ox-PPP and PDH pathways led to the hypothesis that the role of PDH is the supply of reducing equivalents. The finding that a PDH deficiency lowers the NADH : NAD+ ratio supported the proposed role of PDH. Moreover, the NADH : NAD+ ratio in a strain deficient in both PDH and the ox-PPP (Pdh−Zwf−) was even lower than that observed for Pdh−. Strain Pdh−Zwf− also exhibited a slower transition into the exponential phase and a lower growth rate than Pdh−. Finally, a transhydrogenase-deficient strain grew more slowly than wild-type but did not show the slower transition into the exponential phase characteristic of Pdh− mutants. It is proposed that PDH fulfils two metabolic functions. First, by creating the appropriate internal redox state (i.e. appropriate NADH : NAD+ ratio), PDH ensures the functioning of the glucuronate utilization pathway. Secondly, the NADH generated by PDH can be converted to NADPH by the action of transhydrogenases, thus serving as biosynthetic reducing power in the synthesis of building blocks and macromolecules.

scholarly journals Deleted in breast cancer-1 (DBC-1) in the interface between metabolism, aging and cancer

2013 ◽  
Vol 33 (4) ◽  
Author(s):  
Eduardo Nunes Chini ◽  
Claudia C. S. Chini ◽  
Veronica Nin ◽  
Carlos Escande
Keyword(s):  
Breast Cancer ◽  
Molecular Structure ◽  
Energy Metabolism ◽  
Cancer Cell ◽  
Nuclear Protein ◽  
Cellular Metabolism ◽  
New Developments ◽  
Cell Energy ◽  
Cell Energy Metabolism

DBC1 (deleted in breast cancer-1) is a nuclear protein that regulates cellular metabolism. Since alteration in cellular metabolism have been proposed to be the emerging ‘hallmark’ of cancer, it is possible that DBC1 may be implicated in the regulation of cancer cell energy metabolism. However, at this point any role of DBC1 in cancer is only speculative. In this review, we will discuss the new developments in DBC1 research, its molecular structure, regulatory roles and implication in metabolism, aging and cancer.

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