Downregulation of diaphragm electron transport chain and glycolytic enzyme gene expression in sepsis

2005 ◽  
Vol 99 (3) ◽  
pp. 1120-1126 ◽  
Author(s):  
Leigh Ann Callahan ◽  
Gerald S. Supinski
Keyword(s):  
Gene Expression ◽  
Energy Metabolism ◽  
Electron Transport ◽  
Atp Synthase ◽  
Electron Transport Chain ◽  
Cellular Energy ◽  
Protein Levels ◽  
Cellular Energy Metabolism ◽  
Transport Chain ◽  
Genes Encoding

Cellular energy metabolism is altered in sepsis as a consequence of dysfunction of mitochondrial electron transport and glycolytic pathways. The purpose of the present study was to determine whether sepsis is associated with compensatory increases in gene expression of electron transport chain and glycolytic pathway proteins or, alternatively, whether gene expression decreases in sepsis, contributing to abnormalities in energy metabolism. Studies were performed using diaphragms from control and endotoxin-treated (8 mg·kg−1·day−1) rats; at 48 h after endotoxin administration, animals were killed. Microarrays and RNAse protection assays were used to assess the expression of several electron transport chain components (cytochrome- c oxidase subunits Cox 5A, Cox 5B, and Cox 6A, ATP synthase, and ATP synthase subunit 5B) and of the rate-limiting enzyme for glycolysis, phosphofructokinase (PFK). Western blotting was used to assess protein levels for these electron transport chain subunits and PFK. Activity assays were used to assess electron transport chain and phosphofructokinase function. We found that sepsis evoked 1) a downregulation of genes encoding all examined electron transport chain components (e.g., cytochrome- c oxidase 5A decreased 45 + 7%, P < 0.01) and PFK ( P < 0.001), 2) reductions in protein levels for these electron transport chain subunits and PFK ( P < 0.05 for each), and 3) decreases in mitochondrial state 3 respiration rates and phosphofructokinase enzyme activity ( P < 0.01 for each comparison). We speculate that these sepsis-induced reductions in the expression of genes encoding critical electron transport and glycolytic proteins contribute to the development and persistence of sepsis-induced abnormalities in cellular energy metabolism.

scholarly journals The dynamics of mitochondrial-linked gene expression among tissues and life stages in two contrasting strains of laying hens

PLoS ONE ◽  
2022 ◽  
Vol 17 (1) ◽  
pp. e0262613
Author(s):  
Clara Dreyling ◽  
Martin Hasselmann
Keyword(s):  
Gene Expression ◽  
Energy Metabolism ◽  
Life Span ◽  
Laying Hens ◽  
Mitochondrial Gene ◽  
Model Organisms ◽  
Life Stages ◽  
Mitochondrial Gene Expression ◽  
Cellular Energy ◽  
Cellular Energy Metabolism

The cellular energy metabolism is one of the most conserved processes, as it is present in all living organisms. Mitochondria are providing the eukaryotic cell with energy and thus their genome and gene expression has been of broad interest for a long time. Mitochondrial gene expression changes under different conditions and is regulated by genes encoded in the nucleus of the cell. In this context, little is known about non-model organisms and we provide the first large-scaled gene expression analysis of mitochondrial-linked genes in laying hens. We analysed 28 mitochondrial and nuclear genes in 100 individuals in the context of five life-stages and strain differences among five tissues. Our study showed that mitochondrial gene expression increases during the productive life span, and reacts tissue and strain specific. In addition, the strains react different to potential increased oxidative stress, resulting from the increase in mitochondrial gene expression. The results suggest that the cellular energy metabolism as part of a complex regulatory system is strongly affected by the productive life span in laying hens and thus partly comparable to model organisms. This study provides a starting point for further analyses in this field on non-model organisms, especially in laying-hens.

scholarly journals Anesthesia-Sepsis-Associated Alterations in Liver Gene Expression Profiles and Mitochondrial Oxidative Phosphorylation Complexes

2020 ◽  
Vol 7 ◽  
Author(s):  
Hari Prasad Osuru ◽  
Umadevi Paila ◽  
Keita Ikeda ◽  
Zhiyi Zuo ◽  
Robert H. Thiele
Keyword(s):  
Gene Expression ◽  
Electron Transport ◽  
Oxidative Phosphorylation ◽  
Electron Transport Chain ◽  
Expression Profiles ◽  
Volatile Anesthetic ◽  
Heme Oxygenase 1 ◽  
Complex Ii ◽  
Transport Chain ◽  
The Impact

Background: Hepatic dysfunction plays a major role in adverse outcomes in sepsis. Volatile anesthetic agents may protect against organ dysfunction in the setting of critical illness and infection. The goal of this study was to study the impact of Sepsis-inflammation on hepatic subcellular energetics in animals anesthetized with both Propofol (intravenous anesthetic agent and GABA agonist) and Isoflurane (volatile anesthetic i.e., VAA).Methods: Sprague-Dawley rats were anesthetized with Propofol or isoflurane. Rats in each group were randomized to celiotomy and closure (control) or cecal ligation and puncture “CLP” (Sepsis-inflammation) for 8 h.Results: Inflammation led to upregulation in hepatic hypoxia-inducible factor-1 in both groups. Rats anesthetized with isoflurane also exhibited increases in bcl-2, inducible nitric oxide synthase, and heme oxygenase-1(HO-1) during inflammation, whereas rats anesthetized with Propofol did not. In rats anesthetized with isoflurane, decreased mRNA, protein (Complex II, IV, V), and activity levels (Complex II/III,IV,V) were identified for all components of the electron transport chain, leading to a decrease in mitochondrial ATP. In contrast, in rats anesthetized with Propofol, these changes were not identified after exposure to inflammation. RNA-Seq and real-time quantitative PCR (qPCR) expression analysis identified a substantial difference between groups (isoflurane vs. Propofol) in mitogen-activated protein kinase (MAPK) related gene expression following exposure to Sepsis-inflammation.Conclusions: Compared to rats anesthetized with Propofol, those anesthetized with isoflurane exhibit more oxidative stress, decreased oxidative phosphorylation protein expression, and electron transport chain activity and increased expression of organ-protective proteins.

Mitochondrial Disorder for Muscle Biopsy

2013 ◽  
Author(s):  
J. Fay Jou ◽  
Lori A Aronson ◽  
Jacqueline W Morillo-Delerme
Keyword(s):  
Energy Metabolism ◽  
Electron Transport ◽  
Oxidative Phosphorylation ◽  
Mitochondrial Disease ◽  
Electron Transport Chain ◽  
Mitochondrial Disorder ◽  
Metabolic Complications ◽  
Transport Chain ◽  
Increased Risk ◽  
Anesthetic Considerations

Mitochondrial disease (mtD) is a genetically, biochemically, and clinically heterogeneous group of disorders that arise most commonly from defects in the oxidative phosphorylation or electron transport chain involved in energy metabolism. These patients have an increased risk for cardiac, respiratory, neurologic, and metabolic complications from anesthesia. Consequently, there are several anesthetic considerations for patients with mtD.

Functional Expression of Electron Transport Chain and FoF1-ATP Synthase in Optic Nerve Myelin Sheath

2015 ◽  
Vol 40 (11) ◽  
pp. 2230-2241 ◽  
Author(s):  
Martina Bartolucci ◽  
Silvia Ravera ◽  
Greta Garbarino ◽  
Paola Ramoino ◽  
Sara Ferrando ◽  
...  
Keyword(s):  
Electron Transport ◽  
Optic Nerve ◽  
Atp Synthase ◽  
Myelin Sheath ◽  
Electron Transport Chain ◽  
Functional Expression ◽  
Transport Chain ◽  
Fof1 Atp Synthase

scholarly journals Expression of mitochondrial protein genes encoded by nuclear and mitochondrial genomes correlate with energy metabolism in dairy cattle

2020 ◽  
Author(s):  
Jigme Dorji ◽  
Christy J. Vander Jagt ◽  
Josie B. Garner ◽  
Leah C. Marett ◽  
Brett Mason ◽  
...  
Keyword(s):  
Gene Expression ◽  
Energy Metabolism ◽  
Dairy Cattle ◽  
Differential Gene Expression ◽  
High Energy ◽  
Over Expression ◽  
Cellular Energy ◽  
Network Analyses ◽  
Cellular Energy Metabolism ◽  
Differential Gene

Abstract Background Mutations in the mitochondrial genome have been implicated in mitochondrial disease, often characterised by impaired cellular energy metabolism. Cellular energy metabolism in mitochondria involves mitochondrial proteins (MPs) from both the nuclear ( Nu MP) and mitochondrial ( Mt MP) genomes. The expression of MP genes in tissues may be tissue specific to meet varying specific energy demands across the tissues. Currently, the characteristics of MP gene expression in tissues of dairy cattle are not well understood. In this study, we profile the expression of MP genes in 29 adult and six foetal tissues in dairy cattle using RNA sequencing and gene expression analyses: particularly differential gene expression and co-expression network analyses. Results MP genes were differentially expressed (DE; over-expressed or under-expressed) across tissues in cattle. All 29 tissues showed DE Nu MP genes in varying proportions of over-expression and under-expression. On the other hand, DE of Mt MP genes was observed in <50% of tissues and notably Mt MP genes within a tissue was either all over-expressed or all under-expressed . A high proportion of Nu MP (up to 60%) and Mt MP (up to 100%) genes were over-expressed in tissues with expected high metabolic demand; heart, skeletal muscles and tongue, and under-expressed (up to 45% of Nu MP, 77% of Mt MP genes) in tissues with expected low metabolic rates; leukocytes, thymus, and lymph nodes. These tissues also invariably had the expression of all Mt MP genes in the direction of dominant Nu MP genes expression. The Nu MP and Mt MP genes were highly co-expressed across tissues and co-expression of genes in a cluster were non-random and functionally enriched for energy generation pathways. The differential gene expression and co-expression patterns were validated in independent cow and sheep datasets. Conclusions This study demonstrated the biological interaction of MP genes from the mitochondrial and nuclear genomes and their over-expression in tissues with high energy demand. This highlights the importance of considering MP genes from both genomes in future studies related to mitochondrial functions and traits related to energy metabolism.

scholarly journals Effect of heat stress and feeding phosphorus levels on pig electron transport chain gene expression

animal ◽  
2013 ◽  
Vol 7 (12) ◽  
pp. 1985-1993 ◽  
Author(s):  
M.M.D.C.A. Weller ◽  
L. Alebrante ◽  
P.H.R.F. Campos ◽  
A. Saraiva ◽  
B.A.N. Silva ◽  
...  
Keyword(s):  
Gene Expression ◽  
Heat Stress ◽  
Electron Transport ◽  
Electron Transport Chain ◽  
Chain Gene ◽  
Transport Chain ◽  
Phosphorus Levels

The efficiency and plasticity of mitochondrial energy transduction

2005 ◽  
Vol 33 (5) ◽  
pp. 897-904 ◽  
Author(s):  
M.D. Brand
Keyword(s):  
Electron Transport ◽  
Atp Synthase ◽  
Electron Transport Chain ◽  
Uncoupling Protein ◽  
Coupling Efficiency ◽  
Energy Transduction ◽  
Proton Pumping ◽  
Complex Iii ◽  
Proton Pumps ◽  
Transport Chain

Since it was first realized that biological energy transduction involves oxygen and ATP, opinions about the amount of ATP made per oxygen consumed have continually evolved. The coupling efficiency is crucial because it constrains mechanistic models of the electron-transport chain and ATP synthase, and underpins the physiology and ecology of how organisms prosper in a thermodynamically hostile environment. Mechanistically, we have a good model of proton pumping by complex III of the electron-transport chain and a reasonable understanding of complex IV and the ATP synthase, but remain ignorant about complex I. Energy transduction is plastic: coupling efficiency can vary. Whether this occurs physiologically by molecular slipping in the proton pumps remains controversial. However, the membrane clearly leaks protons, decreasing the energy funnelled into ATP synthesis. Up to 20% of the basal metabolic rate may be used to drive this basal leak. In addition, UCP1 (uncoupling protein 1) is used in specialized tissues to uncouple oxidative phosphorylation, causing adaptive thermogenesis. Other UCPs can also uncouple, but are tightly regulated; they may function to decrease coupling efficiency and so attenuate mitochondrial radical production. UCPs may also integrate inputs from different fuels in pancreatic β-cells and modulate insulin secretion. They are exciting potential targets for treatment of obesity, cachexia, aging and diabetes.

scholarly journals Tracking Electron Uptake from a Cathode into Shewanella Cells: Implications for Energy Acquisition from Solid-Substrate Electron Donors

mBio ◽  
2018 ◽  
Vol 9 (1) ◽  
Author(s):  
Annette R. Rowe ◽  
Pournami Rajeev ◽  
Abhiney Jain ◽  
Sahand Pirbadian ◽  
Akihiro Okamoto ◽  
...  
Keyword(s):  
Electron Transfer ◽  
Electron Transport ◽  
Complex I ◽  
Electron Transport Chain ◽  
Electron Flow ◽  
Extracellular Electron Transfer ◽  
Terminal Electron Acceptor ◽  
Cellular Energy ◽  
Transport Chain ◽  
Energy Acquisition

ABSTRACTWhile typically investigated as a microorganism capable of extracellular electron transfer to minerals or anodes,Shewanella oneidensisMR-1 can also facilitate electron flow from a cathode to terminal electron acceptors, such as fumarate or oxygen, thereby providing a model system for a process that has significant environmental and technological implications. This work demonstrates that cathodic electrons enter the electron transport chain ofS. oneidensiswhen oxygen is used as the terminal electron acceptor. The effect of electron transport chain inhibitors suggested that a proton gradient is generated during cathode oxidation, consistent with the higher cellular ATP levels measured in cathode-respiring cells than in controls. Cathode oxidation also correlated with an increase in the cellular redox (NADH/FMNH2) pool determined with a bioluminescence assay, a proton uncoupler, and a mutant of proton-pumping NADH oxidase complex I. This work suggested that the generation of NADH/FMNH2under cathodic conditions was linked to reverse electron flow mediated by complex I. A decrease in cathodic electron uptake was observed in various mutant strains, including those lacking the extracellular electron transfer components necessary for anodic-current generation. While no cell growth was observed under these conditions, here we show that cathode oxidation is linked to cellular energy acquisition, resulting in a quantifiable reduction in the cellular decay rate. This work highlights a potential mechanism for cell survival and/or persistence on cathodes, which might extend to environments where growth and division are severely limited.IMPORTANCEThe majority of our knowledge of the physiology of extracellular electron transfer derives from studies of electrons moving to the exterior of the cell. The physiological mechanisms and/or consequences of the reverse processes are largely uncharacterized. This report demonstrates that when coupled to oxygen reduction, electrode oxidation can result in cellular energy acquisition. This respiratory process has potentially important implications for how microorganisms persist in energy-limited environments, such as reduced sediments under changing redox conditions. From an applied perspective, this work has important implications for microbially catalyzed processes on electrodes, particularly with regard to understanding models of cellular conversion of electrons from cathodes to microbially synthesized products.

Localized energy coupling during photophosphorylation by chromatophores of Rhodopseudomonas capsulata N22

1982 ◽  
Vol 2 (10) ◽  
pp. 743-749 ◽  
Author(s):  
G. Duncan Hitchens ◽  
Douglas B. Kell
Keyword(s):  
Free Energy ◽  
Electron Transport ◽  
Atp Synthase ◽  
Electron Transport Chain ◽  
Energy Coupling ◽  
Rhodopseudomonas Capsulata ◽  
Titration Method ◽  
Dual Inhibitor ◽  
Transport Chain ◽  
Synthase Inhibitor

The principle of the dual inhibitor titration method for testing models of electron-transport phosphorylation is outlined, and the method is applied to the study of photophosphorylation in bacterial chromatophores. It is concluded that energy coupling is strictly localized in nature in this system, in the sense that free energy released by a particular electron-transport chain may be used only by a particular H+-ATP synthase. Dual inhibitor titrations using the uncoupler SF 6847 and the H+-ATP synthase inhibitor oligomycin indicate that uncouplers act by shuttling rapidly between the localized energy-coupling sites.

Sign in / Sign up

Export Citation Format

Share Document