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Cells
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Oxidative Phosphorylation and Hormones: Different Ways of Influence
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Oxidative Phosphorylation and Hormones: Different Ways of Influence

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Signaling".

Deadline for manuscript submissions: closed (31 March 2022) | Viewed by 19410

Special Issue Editors

Dr. Tatiana V. Vygodina

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Guest Editor
Department of Bioenergetics, A.N. Belozersky Institute of Physico-Chemical Biology, M.V. Lomonosov Moscow State University, 119992 Moscow, Russia
Interests: oxidative phosphorylation; mitochondria; respiratory chain; cytochrome oxidase; cytochrome c; reactive oxygen species
Special Issues, Collections and Topics in MDPI journals
Dr. Natalia V. Azarkina

E-Mail Website
Guest Editor
A.N.Belozersky Institute of Physico-Chemical Biology, M.V.Lomonosov Moscow State University, Leninskie gory 1, Bld. 40, 119 992 Moscow, Russia
Interests: bioenergetics; cytochrome oxidase; succinate dehydrogenase; cytochromes; bacterial respiratory chains

Special Issue Information

Dear Colleagues,

A special issue on “Oxidative phosphorylation and hormones: different ways of influence” is planned to be published by the journal “Cells” this year. This issue is intended to compile current information about the ways of hormones influence on the oxidative phosphorylation system (OXPHOS). The hormonal effects on OXPHOS as a whole and its individual components are carried out at different levels, in different cell compartments and by fundamentally different mechanisms. First of all, we would like to focus on thyroid hormones, steroid hormones and compounds structurally close to them in connection with the regulatory function performed by these agents in mitochondria, both via formation of a hormone-receptor complex and directly. Studies comparing the intramitochondrial effects of thyroid and steroid hormones with their other functions (control of nuclear genes expression, participation in the cascade processes in cytoplasm) are welcome. Data on the action of such compounds on the respiratory chain components in prokaryotic cell are also welcome. Studies clarifying the evolutionary meaning of multiple pathways of the OXPHOS hormonal regulation and shedding light on its possible origin would be of particular value.

Dr. Tatiana V. Vygodina
Dr. Natalia V. Azarkina
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • mitochondria
  • respiratory chain
  • steroid hormones
  • thyroid hormones
  • regulation
  • direct and indirect action
  • genomic and non-genomic mechanism

Published Papers (5 papers)

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Research

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21 pages, 3617 KiB  
Article
Direct Interaction of Mitochondrial Cytochrome c Oxidase with Thyroid Hormones: Evidence for Two Binding Sites
by Ilya P. Oleynikov, Roman V. Sudakov, Natalia V. Azarkina and Tatiana V. Vygodina
Cells 2022, 11(5), 908; https://0-doi-org.brum.beds.ac.uk/10.3390/cells11050908 - 6 Mar 2022
Cited by 5 | Viewed by 2010
Abstract
Thyroid hormones regulate tissue metabolism to establish an energy balance in the cell, in particular, by affecting oxidative phosphorylation. Their long-term impact is mainly associated with changes in gene expression, while the short-term effects may differ in their mechanisms. Our work was devoted [...] Read more.
Thyroid hormones regulate tissue metabolism to establish an energy balance in the cell, in particular, by affecting oxidative phosphorylation. Their long-term impact is mainly associated with changes in gene expression, while the short-term effects may differ in their mechanisms. Our work was devoted to studying the short-term effects of hormones T2, T3 and T4 on mitochondrial cytochrome c oxidase (CcO) mediated by direct contact with the enzyme. The data obtained indicate the existence of two separate sites of CcO interaction with thyroid hormones, differing in their location, affinity and specificity to hormone binding. First, we show that T3 and T4 but not T2 inhibit the oxidase activity of CcO in solution and on membrane preparations with Ki ≈ 100–200 μM. In solution, T3 and T4 compete in a 1:1 ratio with the detergent dodecyl-maltoside to bind to the enzyme. The peroxidase and catalase partial activities of CcO are not sensitive to hormones, but electron transfer from heme a to the oxidized binuclear center is affected. We believe that T3 and T4 could be ligands of the bile acid-binding site found in the 3D structure of CcO by Ferguson-Miller’s group, and hormone-induced inhibition is associated with dysfunction of the K-proton channel. A possible role of this interaction in the physiological regulation of the enzyme is discussed. Second, we find that T2, T3, and T4 inhibit superoxide generation by oxidized CcO in the presence of excess H2O2. Inhibition is characterized by Ki values of 0.3–5 μM and apparently affects the formation of O2●− at the protein surface. The second binding site for thyroid hormones presumably coincides with the point of tight T2 binding on the Va subunit described in the literature. Full article
(This article belongs to the Special Issue Oxidative Phosphorylation and Hormones: Different Ways of Influence)
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22 pages, 3832 KiB  
Article
Venlafaxine and L-Thyroxine Treatment Combination: Impact on Metabolic and Synaptic Plasticity Changes in an Animal Model of Coexisting Depression and Hypothyroidism
by Katarzyna Głombik, Jan Detka and Bogusława Budziszewska
Cells 2021, 10(6), 1394; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10061394 - 5 Jun 2021
Cited by 6 | Viewed by 4043
Abstract
The clinical effectiveness of supportive therapy with thyroid hormones in drug-resistant depression is well-known; however, the mechanisms of action of these hormones in the adult brain have not been fully elucidated to date. We determined the effects of venlafaxine and/or L-thyroxine on metabolic [...] Read more.
The clinical effectiveness of supportive therapy with thyroid hormones in drug-resistant depression is well-known; however, the mechanisms of action of these hormones in the adult brain have not been fully elucidated to date. We determined the effects of venlafaxine and/or L-thyroxine on metabolic parameters and markers involved in the regulation of synaptic plasticity and cell damage in an animal model of coexisting depression and hypothyroidism, namely, Wistar Kyoto rats treated with propylthiouracil. In this model, in relation to the depression model itself, the glycolysis process in the brain was weakened, and a reduction in pyruvate dehydrogenase in the frontal cortex was normalized only by the combined treatment with L-thyroxine and venlafaxine, whereas changes in pyruvate and lactate levels were affected by all applied therapies. None of the drugs improved the decrease in the expression of mitochondrial respiratory chain enzymes. No intensification of glucocorticoid action was shown, while an unfavorable change caused by the lack of thyroid hormones was an increase in the caspase-1 level, which was not reversed by venlafaxine alone. The results indicated that the combined administration of drugs was more effective in normalizing glycolysis and the transition to the Krebs cycle than the use of venlafaxine or L-thyroxine alone. Full article
(This article belongs to the Special Issue Oxidative Phosphorylation and Hormones: Different Ways of Influence)
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21 pages, 7499 KiB  
Article
Lysine 53 Acetylation of Cytochrome c in Prostate Cancer: Warburg Metabolism and Evasion of Apoptosis
by Viktoriia Bazylianska, Hasini A. Kalpage, Junmei Wan, Asmita Vaishnav, Gargi Mahapatra, Alice A. Turner, Dipanwita Dutta Chowdhury, Katherine Kim, Paul T. Morse, Icksoo Lee, Joseph S. Brunzelle, Lisa Polin, Prabal Subedi, Elisabeth I. Heath, Izabela Podgorski, Katrin Marcus, Brian F.P. Edwards and Maik Hüttemann
Cells 2021, 10(4), 802; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10040802 - 3 Apr 2021
Cited by 18 | Viewed by 3367
Abstract
Prostate cancer is the second leading cause of cancer-related death in men. Two classic cancer hallmarks are a metabolic switch from oxidative phosphorylation (OxPhos) to glycolysis, known as the Warburg effect, and resistance to cell death. Cytochrome c (Cytc) is at [...] Read more.
Prostate cancer is the second leading cause of cancer-related death in men. Two classic cancer hallmarks are a metabolic switch from oxidative phosphorylation (OxPhos) to glycolysis, known as the Warburg effect, and resistance to cell death. Cytochrome c (Cytc) is at the intersection of both pathways, as it is essential for electron transport in mitochondrial respiration and a trigger of intrinsic apoptosis when released from the mitochondria. However, its functional role in cancer has never been studied. Our data show that Cytc is acetylated on lysine 53 in both androgen hormone-resistant and -sensitive human prostate cancer xenografts. To characterize the functional effects of K53 modification in vitro, K53 was mutated to acetylmimetic glutamine (K53Q), and to arginine (K53R) and isoleucine (K53I) as controls. Cytochrome c oxidase (COX) activity analyzed with purified Cytc variants showed reduced oxygen consumption with acetylmimetic Cytc compared to the non-acetylated Cytc (WT), supporting the Warburg effect. In contrast to WT, K53Q Cytc had significantly lower caspase-3 activity, suggesting that modification of Cytc K53 helps cancer cells evade apoptosis. Cardiolipin peroxidase activity, which is another proapoptotic function of the protein, was lower in acetylmimetic Cytc. Acetylmimetic Cytc also had a higher capacity to scavenge reactive oxygen species (ROS), another pro-survival feature. We discuss our experimental results in light of structural features of K53Q Cytc, which we crystallized at a resolution of 1.31 Å, together with molecular dynamics simulations. In conclusion, we propose that K53 acetylation of Cytc affects two hallmarks of cancer by regulating respiration and apoptosis in prostate cancer xenografts. Full article
(This article belongs to the Special Issue Oxidative Phosphorylation and Hormones: Different Ways of Influence)
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Review

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22 pages, 1153 KiB  
Review
Bioenergetic Aspects of Mitochondrial Actions of Thyroid Hormones
by Federica Cioffi, Antonia Giacco, Fernando Goglia and Elena Silvestri
Cells 2022, 11(6), 997; https://0-doi-org.brum.beds.ac.uk/10.3390/cells11060997 - 15 Mar 2022
Cited by 18 | Viewed by 4749
Abstract
Much is known, but there is also much more to discover, about the actions that thyroid hormones (TH) exert on metabolism. Indeed, despite the fact that thyroid hormones are recognized as one of the most important regulators of metabolic rate, much remains to [...] Read more.
Much is known, but there is also much more to discover, about the actions that thyroid hormones (TH) exert on metabolism. Indeed, despite the fact that thyroid hormones are recognized as one of the most important regulators of metabolic rate, much remains to be clarified on which mechanisms control/regulate these actions. Given their actions on energy metabolism and that mitochondria are the main cellular site where metabolic transformations take place, these organelles have been the subject of extensive investigations. In relatively recent times, new knowledge concerning both thyroid hormones (such as the mechanisms of action, the existence of metabolically active TH derivatives) and the mechanisms of energy transduction such as (among others) dynamics, respiratory chain organization in supercomplexes and cristes organization, have opened new pathways of investigation in the field of the control of energy metabolism and of the mechanisms of action of TH at cellular level. In this review, we highlight the knowledge and approaches about the complex relationship between TH, including some of their derivatives, and the mitochondrial respiratory chain. Full article
(This article belongs to the Special Issue Oxidative Phosphorylation and Hormones: Different Ways of Influence)
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28 pages, 5238 KiB  
Review
Hormonal Regulation of Oxidative Phosphorylation in the Brain in Health and Disease
by Katarzyna Głombik, Jan Detka and Bogusława Budziszewska
Cells 2021, 10(11), 2937; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10112937 - 28 Oct 2021
Cited by 13 | Viewed by 4273
Abstract
The developing and adult brain is a target organ for the vast majority of hormones produced by the body, which are able to cross the blood–brain barrier and bind to their specific receptors on neurons and glial cells. Hormones ensure proper communication between [...] Read more.
The developing and adult brain is a target organ for the vast majority of hormones produced by the body, which are able to cross the blood–brain barrier and bind to their specific receptors on neurons and glial cells. Hormones ensure proper communication between the brain and the body by activating adaptive mechanisms necessary to withstand and react to changes in internal and external conditions by regulating neuronal and synaptic plasticity, neurogenesis and metabolic activity of the brain. The influence of hormones on energy metabolism and mitochondrial function in the brain has gained much attention since mitochondrial dysfunctions are observed in many different pathological conditions of the central nervous system. Moreover, excess or deficiency of hormones is associated with cell damage and loss of function in mitochondria. This review aims to expound on the impact of hormones (GLP-1, insulin, thyroid hormones, glucocorticoids) on metabolic processes in the brain with special emphasis on oxidative phosphorylation dysregulation, which may contribute to the formation of pathological changes. Since the brain concentrations of sex hormones and neurosteroids decrease with age as well as in neurodegenerative diseases, in parallel with the occurrence of mitochondrial dysfunction and the weakening of cognitive functions, their beneficial effects on oxidative phosphorylation and expression of antioxidant enzymes are also discussed. Full article
(This article belongs to the Special Issue Oxidative Phosphorylation and Hormones: Different Ways of Influence)
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