scholarly journals Mechanistic Target of Rapamycin Complex 1 Promotes the Expression of Genes Encoding Electron Transport Chain Proteins and Stimulates Oxidative Phosphorylation in Primary Human Trophoblast Cells by Regulating Mitochondrial Biogenesis

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Fredrick J. Rosario ◽  
Madhulika B. Gupta ◽  
Leslie Myatt ◽  
Theresa L. Powell ◽  
Jeremy P. Glenn ◽  
...  
Keyword(s):  
Electron Transport ◽  
Oxidative Phosphorylation ◽  
Mitochondrial Biogenesis ◽  
Electron Transport Chain ◽  
Human Trophoblast ◽  
Mechanistic Target Of Rapamycin ◽  
Expression Of Genes ◽  
Transport Chain ◽  
Genes Encoding ◽  
Human Trophoblast Cells

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.

scholarly journals Stress signalling dynamics of the mitochondrial electron transport chain and oxidative phosphorylation system in higher plants

2019 ◽  
Vol 125 (5) ◽  
pp. 721-736 ◽  
Author(s):  
Corentin Dourmap ◽  
Solène Roque ◽  
Amélie Morin ◽  
Damien Caubrière ◽  
Margaux Kerdiles ◽  
...  
Keyword(s):  
Climate Change ◽  
Electron Transport ◽  
Oxidative Phosphorylation ◽  
Electron Transport Chain ◽  
Plant Mitochondria ◽  
Mitochondrial Electron Transport Chain ◽  
Oxidative Phosphorylation System ◽  
Transport Chain ◽  
Wide Range ◽  
Stress Signalling

Abstract Background Mitochondria play a diversity of physiological and metabolic roles under conditions of abiotic or biotic stress. They may be directly subjected to physico-chemical constraints, and they are also involved in integrative responses to environmental stresses through their central position in cell nutrition, respiration, energy balance and biosyntheses. In plant cells, mitochondria present various biochemical peculiarities, such as cyanide-insensitive alternative respiration, and, besides integration with ubiquitous eukaryotic compartments, their functioning must be coupled with plastid functioning. Moreover, given the sessile lifestyle of plants, their relative lack of protective barriers and present threats of climate change, the plant cell is an attractive model to understand the mechanisms of stress/organelle/cell integration in the context of environmental stress responses. Scope The involvement of mitochondria in this integration entails a complex network of signalling, which has not been fully elucidated, because of the great diversity of mitochondrial constituents (metabolites, reactive molecular species and structural and regulatory biomolecules) that are linked to stress signalling pathways. The present review analyses the complexity of stress signalling connexions that are related to the mitochondrial electron transport chain and oxidative phosphorylation system, and how they can be involved in stress perception and transduction, signal amplification or cell stress response modulation. Conclusions Plant mitochondria are endowed with a diversity of multi-directional hubs of stress signalling that lead to regulatory loops and regulatory rheostats, whose functioning can amplify and diversify some signals or, conversely, dampen and reduce other signals. Involvement in a wide range of abiotic and biotic responses also implies that mitochondrial stress signalling could result in synergistic or conflicting outcomes during acclimation to multiple and complex stresses, such as those arising from climate change.

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.

scholarly journals PGC1α and Exercise Adaptations in Zebrafish

2018 ◽  
Author(s):  
Alice Parisi ◽  
Peter Blattmann ◽  
Giulia Lizzo ◽  
Vivienne Stutz ◽  
Laura Strohm ◽  
...  
Keyword(s):  
Electron Transport ◽  
Physical Fitness ◽  
Mitochondrial Biogenesis ◽  
Electron Transport Chain ◽  
Supramolecular Complex ◽  
List Type ◽  
Complex Iv ◽  
Transport Chain ◽  
Response To Exercise

ABSTRACTFish species display huge differences in physical activity ranging from lethargy to migration of thousands of miles, making them an interesting model to identify determinants of physical fitness. Here, we show a remarkable plasticity of zebrafish in response to exercise and induction of PGC1α (encoded by PPARGC1A), a dominant regulator of mitochondrial biogenesis. Forced expression of human PPARGC1A induces mitochondrial biogenesis, an exercise-like gene expression signature, and physical fitness comparable to wild-type animals trained in counter-current swim tunnels. Quantifying transcriptional and proteomic changes in response to exercise or PGC1α, we identify conserved ‘exercise’ adaptations, including a stoichiometric induction of the electron transport chain (ETC) that re-organizes into respiratory supercomplexes in both conditions. We further show that ndufa4/ndufa4l, previously assigned to complex I, associates to free and supramolecular complex IV in vivo. Thus, zebrafish is a useful and experimentally tractable vertebrate model to study exercise biology, including ETC expression and assembly.HIGHLIGHTSPGC1α reprograms zebrafish skeletal muscle to a ‘red fiber’ phenotype and increases exercise performanceZebrafish show a high molecular plasticity in response to PGC1α and exerciseSWATH-MS proteomics show a stoichiometric induction of the electron transport chain that organizes as supercomplexes in response to PGC1α and exercisendufa4/ndufa4l associate to free and supramolecular complex IV in vivo

scholarly journals FOXM1 nuclear transcription factor translocates into mitochondria and inhibits oxidative phosphorylation

2020 ◽  
Vol 31 (13) ◽  
pp. 1411-1424
Author(s):  
Markaisa Black ◽  
Paritha Arumugam ◽  
Samriddhi Shukla ◽  
Arun Pradhan ◽  
Vladimir Ustiyan ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Membrane Potential ◽  
Electron Transport ◽  
Oxidative Phosphorylation ◽  
Mitochondrial Respiration ◽  
Electron Transport Chain ◽  
Nuclear Transcription Factor ◽  
Transport Chain

It was found that the transcription factor FOXM1 translocates into mitochondria and inhibits mitochondrial respiration and membrane potential, directly binds to mitochondrial PTCD1, and inhibits the electron transport chain by stabilizing PTCD1.

scholarly journals CtaM Is Required for Menaquinol Oxidaseaa3Function inStaphylococcus aureus

mBio ◽  
2016 ◽  
Vol 7 (4) ◽  
Author(s):  
Neal D. Hammer ◽  
Lici A. Schurig-Briccio ◽  
Svetlana Y. Gerdes ◽  
Robert B. Gennis ◽  
Eric P. Skaar
Keyword(s):  
Staphylococcus Aureus ◽  
Electron Transport ◽  
Electron Transport Chain ◽  
Molecular Mechanisms ◽  
Carbon Sources ◽  
Spectroscopic Studies ◽  
Uncharacterized Protein ◽  
Terminal Oxidases ◽  
Transport Chain ◽  
Genes Encoding

ABSTRACTStaphylococcus aureusis the leading cause of skin and soft tissue infections, bacteremia, osteomyelitis, and endocarditis in the developed world. The ability ofS. aureusto cause substantial disease in distinct host environments is supported by a flexible metabolism that allows this pathogen to overcome challenges unique to each host organ. One feature of staphylococcal metabolic flexibility is a branched aerobic respiratory chain composed of multiple terminal oxidases. Whereas previous biochemical and spectroscopic studies reported the presence of three different respiratory oxygen reductases (otype,bdtype, andaa3type), the genome contains genes encoding only two respiratory oxygen reductases,cydABandqoxABCD. Previous investigation showed thatcydABandqoxABCDare required to colonize specific host organs, the murine heart and liver, respectively. This work seeks to clarify the relationship between the genetic studies showing the unique roles of thecydABandqoxABCDin virulence and the respiratory reductases reported in the literature. We establish that QoxABCD is anaa3-type menaquinol oxidase but that this enzyme is promiscuous in that it can assemble as abo3-type menaquinol oxidase. However, thebo3form of QoxABCD restricts the carbon sources that can support the growth ofS. aureus. In addition, QoxABCD function is supported by a previously uncharacterized protein, which we have named CtaM, that is conserved in aerobically respiringFirmicutes. In total, these studies establish the heme A biosynthesis pathway inS. aureus, determine that QoxABCD is a typeaa3menaquinol oxidase, and reveal CtaM as a new protein required for typeaa3menaquinol oxidase function in multiple bacterial genera.IMPORTANCEStaphylococcus aureusrelies upon the function of two terminal oxidases, CydAB and QoxABCD, to aerobically respire and colonize distinct host tissues. Previous biochemical studies support the conclusion that a third terminal oxidase is also present. We establish the components of theS. aureuselectron transport chain by determining the heme cofactors that interact with QoxABCD. This insight explains previous observations by revealing that QoxABCD can utilize different heme cofactors and confirms that the electron transport chain ofS. aureusis comprised of two terminal menaquinol oxidases. In addition, a newly identified protein, CtaM, is found to be required for the function of QoxABCD. These results provide a more complete assessment of the molecular mechanisms that support staphylococcal respiration.

scholarly journals Mechanistic Target of Rapamycin Complex 2 Regulation of the Primary Human Trophoblast Cell Transcriptome

2021 ◽  
Vol 9 ◽  
Author(s):  
Fredrick J. Rosario ◽  
Amy Catherine Kelly ◽  
Madhulika B. Gupta ◽  
Theresa L. Powell ◽  
Laura Cox ◽  
...  
Keyword(s):  
Protein Expression ◽  
Gene Array ◽  
Target Of Rapamycin ◽  
Human Trophoblast ◽  
Mechanistic Target Of Rapamycin ◽  
Expression Of Genes ◽  
Genes Encoding ◽  
Cell Transcriptome ◽  
Pathway Analyses

Mechanistic Target of Rapamycin Complex 2 (mTORC2) regulates placental amino acid and folate transport. However, the role of mTORC2 in modulating other placental functions is largely unexplored. We used a gene array following the silencing of rictor to identify genes regulated by mTORC2 in primary human trophoblast (PHT) cells. Four hundred and nine genes were differentially expressed; 102 genes were down-regulated and 307 up-regulated. Pathway analyses demonstrated that inhibition of mTORC2 resulted in increased expression of genes encoding for pro-inflammatory IL-6, VEGF-A, leptin, and inflammatory signaling (SAPK/JNK). Furthermore, down-regulated genes were functionally enriched in genes involved in angiogenesis (Osteopontin) and multivitamin transport (SLC5A6). In addition, the protein expression of leptin, VEGFA, IL-6 was increased and negatively correlated to mTORC2 signaling in human placentas collected from pregnancies complicated by intrauterine growth restriction (IUGR). In contrast, the protein expression of Osteopontin and SLC5A6 was decreased and positively correlated to mTORC2 signaling in human IUGR placentas. In conclusion, mTORC2 signaling regulates trophoblast expression of genes involved in inflammation, micronutrient transport, and angiogenesis, representing novel links between mTOR signaling and multiple placental functions necessary for fetal growth and development.

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