Relevant bibliographies by topics / Adaptation mitochondriale

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Academic literature on the topic 'Adaptation mitochondriale'

Author: Grafiati
Published: 18 May 2024

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Journal articles on the topic "Adaptation mitochondriale"

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Calmettes, G., V. Deschodt-Arsac, E. Thiaudiere, S. Miraux, B. Muller, and P. Diolez. "F008 Adaptation de l’énergétique mitochondriale cardiaque chez la souris en réponse à l’hypoxie chronique." Archives of Cardiovascular Diseases 102 (March 2009): S55—S56. http://dx.doi.org/10.1016/s1875-2136(09)72261-2.

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Adhihetty, Peter J., Vladimir Ljubicic, and David A. Hood. "Effect of chronic contractile activity on SS and IMF mitochondrial apoptotic susceptibility in skeletal muscle." American Journal of Physiology-Endocrinology and Metabolism 292, no. 3 (March 2007): E748—E755. http://dx.doi.org/10.1152/ajpendo.00311.2006.

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Chronic contractile activity of skeletal muscle induces an increase in mitochondria located in proximity to the sarcolemma [subsarcolemmal (SS)] and in mitochondria interspersed between the myofibrils [intermyofibrillar (IMF)]. These are energetically favorable metabolic adaptations, but because mitochondria are also involved in apoptosis, we investigated the effect of chronic contractile activity on mitochondrially mediated apoptotic signaling in muscle. We hypothesized that chronic contractile activity would provide protection against mitochondrially mediated apoptosis despite an elevation in the expression of proapoptotic proteins. To induce mitochondrial biogenesis, we chronically stimulated (10 Hz; 3 h/day) rat muscle for 7 days. Chronic contractile activity did not alter the Bax/Bcl-2 ratio, an index of apoptotic susceptibility, and did not affect manganese superoxide dismutase levels. However, contractile activity increased antiapoptotic 70-kDa heat shock protein and apoptosis repressor with a caspase recruitment domain by 1.3- and 1.4-fold ( P < 0.05), respectively. Contractile activity elevated SS mitochondrial reactive oxygen species (ROS) production 1.4- and 1.9-fold ( P < 0.05) during states IV and III respiration, respectively, whereas IMF mitochondrial state IV ROS production was suppressed by 28% ( P < 0.05) and was unaffected during state III respiration. Following stimulation, exogenous ROS treatment produced less cytochrome c release (25–40%) from SS and IMF mitochondria, and also reduced apoptosis-inducing factor release (≈30%) from IMF mitochondria, despite higher inherent cytochrome c and apoptosis-inducing factor expression. Chronic contractile activity did not alter mitochondrial permeability transition pore (mtPTP) components in either subfraction. However, SS mitochondria exhibited a significant increase in the time to Vmax of mtPTP opening. Thus, chronic contractile activity induces predominantly antiapoptotic adaptations in both mitochondrial subfractions. Our data suggest the possibility that chronic contractile activity can exert a protective effect on mitochondrially mediated apoptosis in muscle.
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Tobler, M., N. Barts, and R. Greenway. "Mitochondria and the Origin of Species: Bridging Genetic and Ecological Perspectives on Speciation Processes." Integrative and Comparative Biology 59, no. 4 (April 20, 2019): 900–911. http://dx.doi.org/10.1093/icb/icz025.

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Abstract Mitochondria have been known to be involved in speciation through the generation of Dobzhansky–Muller incompatibilities, where functionally neutral co-evolution between mitochondrial and nuclear genomes can cause dysfunction when alleles are recombined in hybrids. We propose that adaptive mitochondrial divergence between populations can not only produce intrinsic (Dobzhansky–Muller) incompatibilities, but could also contribute to reproductive isolation through natural and sexual selection against migrants, post-mating prezygotic isolation, as well as by causing extrinsic reductions in hybrid fitness. We describe how these reproductive isolating barriers can potentially arise through adaptive divergence of mitochondrial function in the absence of mito-nuclear coevolution, a departure from more established views. While a role for mitochondria in the speciation process appears promising, we also highlight critical gaps of knowledge: (1) many systems with a potential for mitochondrially-mediated reproductive isolation lack crucial evidence directly linking reproductive isolation and mitochondrial function; (2) it often remains to be seen if mitochondrial barriers are a driver or a consequence of reproductive isolation; (3) the presence of substantial gene flow in the presence of mito-nuclear incompatibilities raises questions whether such incompatibilities are strong enough to drive speciation to completion; and (4) it remains to be tested how mitochondrial effects on reproductive isolation compare when multiple mechanisms of reproductive isolation coincide. We hope this perspective and the proposed research plans help to inform future studies of mitochondrial adaptation in a manner that links genotypic changes to phenotypic adaptations, fitness, and reproductive isolation in natural systems, helping to clarify the importance of mitochondria in the formation and maintenance of biological diversity.
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Assayag, Miri, Ann Saada, Gary Gerstenblith, Haifa Canaana, Rivka Shlomai, and Michal Horowitz. "Mitochondrial performance in heat acclimation—a lesson from ischemia/reperfusion and calcium overload insults in the heart." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 303, no. 8 (October 15, 2012): R870—R881. http://dx.doi.org/10.1152/ajpregu.00155.2012.

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Long-term heat acclimation (LTHA; 30 days, 34°C) causes phenotypic adaptations that render protection against ischemic/reperfusion insult (I/R, 30 min global ischemia and 40 min reperfusion) via heat acclimation-mediated cross-tolerance (HACT) mechanisms. Short-term acclimation (STHA, 2 days, 34°C), in contrast, is characterized by cellular perturbations, leading to increased susceptibility to insults. Here, we tested the hypothesis that enhanced mitochondrial respiratory function is part of the acclimatory repertoire and that the 30-day regimen is required for protection via HACT. We subjected isolated hearts and mitochondria from controls (C), STHA, or LTHA rats to I/R, hypoxia/reoxygenation, or Ca2+ overload insults. Mitochondrial function was assessed by measuring O2 consumption, membrane potential (ΔΨm), mitochondrial Ca2+ ([Ca2+]m), ATP production, respiratory chain complex activities, and molecular markers of mitochondrial biogenesis. Our results, combining physiological and biochemical parameters, confirmed that mitochondria from LTHA rats subjected to insults, in contrast to C, preserve respiratory functions (e.g., upon I/R, C mitochondria fueled by glutamate-malate, demonstrated decreases of 81%, 13%, 25%, and 50% in O2/P ratio, ATP production, ΔΨm, and complex I activity, respectively, whereas the corresponding LTHA parameters remained unchanged). STHA mitochondria maintained ΔΨm but did not preserve ATP production. LTHA [Ca2+]m was significantly higher than that of C and STHA and was not affected by the hypoxia/reoxygenation protocol compared with C. Enhanced mitochondrial biogenesis markers, switched-on during STHA coincidentally with enhanced membrane integrity (ΔΨm), were insufficient to confer intact respiratory function upon insult. LTHA was required for respiratory complex I adaptation and HACT. Stabilized higher basal [Ca2+]m and attenuated Ca2+ overload are likely connected to this adaptation.
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Li, Busu, Huan Wang, Xianghui Zeng, Shufang Liu, and Zhimeng Zhuang. "Mitochondrial Homeostasis Regulating Mitochondrial Number and Morphology Is a Distinguishing Feature of Skeletal Muscle Fiber Types in Marine Teleosts." International Journal of Molecular Sciences 25, no. 3 (January 26, 2024): 1512. http://dx.doi.org/10.3390/ijms25031512.

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Fishes’ skeletal muscles are crucial for swimming and are differentiated into slow-twitch muscles (SM) and fast-twitch muscles (FM) based on physiological and metabolic properties. Consequently, mitochondrial characteristics (number and morphology) adapt to each fiber type’s specific functional needs. However, the mechanisms governing mitochondrial adaptation to the specific bioenergetic requirements of each fiber type in teleosts remain unclear. To address this knowledge gap, we investigated the mitochondrial differences and mitochondrial homeostasis status (including biogenesis, autophagy, fission, and fusion) between SM and FM in teleosts using Takifugu rubripes as a representative model. Our findings reveal that SM mitochondria are more numerous and larger compared to FM. To adapt to the increased mitochondrial number and size, SM exhibit elevated mitochondrial biogenesis and dynamics (fission/fusion), yet show no differences in mitochondrial autophagy. Our study provides insights into the adaptive mechanisms shaping mitochondrial characteristics in teleost muscles. The abundance and elongation of mitochondria in SM are maintained through elevated mitochondrial biogenesis, fusion, and fission, suggesting an adaptive response to fulfill the bioenergetic demands of SM that rely extensively on OXPHOS in teleosts. Our findings enhance our understanding of mitochondrial adaptations in diverse muscle types among teleosts and shed light on the evolutionary strategies of bioenergetics in fishes.
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Hokayem, M., K. Lambert, J. F. Brun, C. Fedou, E. Blond, C. Coudray, J. P. Cristol, A. M. Dupuy, M. Laville, and A. Avignon. "O06 L’augmentation de la glycémie s’accompagne d’une adaptation de la fonction mitochondriale dans une population apparentée au 1er degré à des diabétiques de type 2." Cahiers de Nutrition et de Diététique 46 (December 2011): S23—S24. http://dx.doi.org/10.1016/s0007-9960(11)70027-x.

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Hokayem, M., K. Lambert, J. F. Brun, C. Fedou, E. Blond, C. Coudray, J. P. Cristol, A. M. Dupuy, M. Laville, and A. Avignon. "O06 L’augmentation de la glycémie s’accompagne d’une adaptation de la fonction mitochondriale dans une population apparentée au 1er degré à des diabétiques de type 2." Nutrition Clinique et Métabolisme 25 (December 2011): S23—S24. http://dx.doi.org/10.1016/s0985-0562(11)70010-3.

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Ojuka, Edward O. "Role of calcium and AMP kinase in the regulation of mitochondrial biogenesis and GLUT4 levels in muscle." Proceedings of the Nutrition Society 63, no. 2 (May 2004): 275–78. http://dx.doi.org/10.1079/pns2004339.

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Contractile activity induces mitochondrial biogenesis and increases glucose transport capacity in muscle. There has been much research on the mechanisms responsible for these adaptations. The present paper reviews the evidence, which indicates that the decrease in the levels of high-energy phosphates, leading to activation of AMP kinase (AMPK), and the increase in cytosolic Ca2+, which activates Ca2+/calmodulin-dependent protein kinase (CAMK), are signals that initiate these adaptative responses. Although the events downstream of AMPK and CAMK have not been well characterized, these events lead to activation of various transcription factors, including: nuclear respiratory factors (NRF) 1 and 2, which cause increased expression of proteins of the respiratory chain; PPAR-α, which up regulates the levels of enzymes of β oxidation; mitochondrial transcription factor A, which activates expression of the mitochondrial genome; myocyte-enhancing factor 2A, the transcription factor that regulates GLUT4 expression. The well-orchestrated expression of the multitude of proteins involved in these adaptations is mediated by the rapid activation of PPARγ co-activator (PGC) 1, a protein that binds to various transcription factors to maximize transcriptional activity. Activating AMPK using 5-aminoimidizole-4-carboxamide-1-β-D-riboside (AICAR) and increasing cytoplasmic Ca2+using caffeine, W7 or ionomycin in L6 myotubes increases the concentration of mitochondrial enzymes and GLUT4 and enhances the binding of NRF-1 and NRF-2 to DNA. AICAR and Ca-releasing agents also increase the levels of PGC-1, mitochondrial transcription factor A and myocyte-enhancing factors 2A and 2D. These results are similar to the responses seen in muscle during the adaptation to endurance exercise and show that L6 myotubes are a suitable model for studying the mechanisms by which exercise causes the adaptive responses in muscle mitochondria and glucose transport.
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Ballantyne, J. S., and M. E. Chamberlin. "Adaptation and evolution of mitochondria: osmotic and ionic considerations." Canadian Journal of Zoology 66, no. 5 (May 1, 1988): 1028–35. http://dx.doi.org/10.1139/z88-152.

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Mitochondrial evolution has been examined on the basis of properties of mitochondria from representatives of key adaptive stages. The major step in the evolution of mitochondria was the transfer of mitochondrial genes to the nucleus to take advantage of recombination during meiosis. The ensuing increase in variability facilitated adaptation to environmental stress. The role of environmental factors such as atmospheric oxygen levels in the evolution of mitochondria is discussed on the basis of evidence obtained from mitochondria of living representatives of important groups and the fossil record. Rate enhancement has been a central theme in the evolution of animal mitochondria. Optimization of mitochondrial oxidation rates occurred through adjustments in intracellular solute systems. This took place in several stages, including (i) a reduction of intracellular inorganic ion levels by substitution of a variety of compatible solutes, (ii) a counteracting solute system (urea and methylamines), and (iii) osmoregulation.
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Johnston, I. A., H. Guderley, C. E. Franklin, T. Crockford, and C. Kamunde. "ARE MITOCHONDRIA SUBJECT TO EVOLUTIONARY TEMPERATURE ADAPTATION?" Journal of Experimental Biology 195, no. 1 (October 1, 1994): 293–306. http://dx.doi.org/10.1242/jeb.195.1.293.

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Thermal tolerance and the respiratory properties of isolated red muscle mitochondria were investigated in Oreochromis alcalicus grahami from the alkaline hot-springs, Lake Magadi, Kenya. Populations of O. a. grahami were resident in pools at 42.8 &deg;C and migrated into water reaching temperatures of 44.8 &deg;C for short periods. The maximum respiration rates of mitochondria with pyruvate as substrate were 217 and 284 natom O mg-1 mitochondrial protein min-1 at 37 &deg;C and 42 &deg;C, respectively (Q10=1.71). Fatty acyl carnitines (chain lengths C8, C12 and C16), malate and glutamate were oxidised at 70&shy;80 % of the rate for pyruvate. In order to assess evolutionary temperature adaptation of maximum mitochondrial oxidative capacities, the rates of pyruvate and palmitoyl carnitine utilisation in red muscle mitochondria were measured from species living at other temperatures: Notothenia coriiceps from Antarctica (-1.5 to +1 &deg;C); summer-caught Myoxocephalus scorpius from the North Sea (10&shy;15 &deg;C); and Oreochromis andersoni from African lakes and rivers (22&shy;30 &deg;C). State 3 respiration rates had Q10 values in the range 1.8&shy;2.7. At the lower lethal temperature of O. andersoni (12.5 &deg;C), isolated mitochondria utilised pyruvate at a similar rate to mitochondria from N. coriiceps at 2.5 &deg;C (30 natom O mg-1 mitochondrial protein min-1). Rates of pyruvate oxidation by mitochondria from M. scorpius and N. coriiceps were similar and were higher at a given temperature than for O. andersoni. At their normal body temperature (-1.2 &deg;C), mitochondria from the Antarctic fish oxidised pyruvate at 5.5 % and palmitoyl-dl-carnitine at 8.8 % of the rates of mitochondria from the hot-spring species at 42 &deg;C. The results indicate only modest evolutionary adjustments in the maximal rates of mitochondrial respiration in fish living at different temperatures.
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Dissertations / Theses on the topic "Adaptation mitochondriale"

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N'Guessan, Banga Benoît. "Traitement immunosuppresseur et muscles striés : évaluation et adaptation de la fonction mitochondriale du sujet transplanté cardiaque." Université Louis Pasteur (Strasbourg) (1971-2008), 2003. https://publication-theses.unistra.fr/public/theses_doctorat/2003/NGUESSAN_Banga_Benoit_2003_ED414.pdf.

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Malgré la quasi-normalisation de sa fonction cardiaque, le sujet transplanté cardiaque présente généralement une limitation à l'effort physique. Ce handicap a été attribué en partie à des altérations du métabolisme énergétique musculaire périphérique, dont les causes précises restent encore à élucider. Cependant, le traitement immunosuppresseur (la ciclosporine en particulier) et le déconditionnement physique, ont été fortement suspectés d'être à l'origine des anomalies musculaires du transplanté. L'objectif de ce travail de thèse était donc de déterminer les parts respectives de la ciclosporine et du déconditionnement dans cette limitation physique. Pour ce faire, nous avons étudié les caractéristiques phénotypiques et fonctionnelles de leurs muscles squelettique et cardiaque, et évalué les effets d'un entraînement en endurance sur ces divers paramètres. Nos résultats démontrent que les capacités oxydatives musculaires du sujet transplanté cardiaque ne varient pas significativement près d'un an après transplantation et demeurent similaires à celles de sujets sédentaires sains appariés en âge. Cependant, in vitro, la CsA (Sandimmun), entraîne une diminution de ces capacités oxydatives, entièrement attribuable au composant majeur de son excipient, le Crémophor. Cet effet délétère est tissue-spécifique et s'exerce via une altération spécifique de l'activité fonctionnelle de certains complexes de la chaîne respiratoire mitochondriale. Par ailleurs, l'administration chronique de la molécule active de CsA, sans son excipient, entraîne au contraire, une augmentation de la capacité oxydative du muscle squelettique lent oxydatif. L'entraînement en endurance de ces sujets induit une augmentation significative de la capacité oxydative du muscle squelettique (dont la valeur devient même similaire à celle du sujet sain sportif) associée à une activation fonctionnelle de la créatine kinase mitochondriale. L'ensemble de notre travail suggère que la fonction mitochondriale musculaire et ses mécanismes de régulation soient préservés in vivo, malgré le traitement immunosuppresseur clinique. D'autres acteurs, extramitochondriaux, tels que le réseau capillaire et certaines voies de signalisation impliquées dans la transition phénotypique musculaire, seraient les cibles préférentielles des immunosuppresseurs
Despite a near-normalization of their cardiac function, heart transplant recipient displayed a limited physical capacity, at maximal exercise. This physical limitation has been in part attributed to altered energetical metabolism in peripheral muscle, which precise mechanisms are still undetermined. However, immunosuppressive treatment, particularly cyclosporin A, and deconditionning have been closely suspected to be the major causes of muscular abnormalities after cardiac transplantation. The aim of this study was to determine the respective contribution of cyclosporin A and deconditionning in physical limitation of heart transplant recipient. To this end, we have characterized the phenotypic and functional properties of their skeletal and cardiac muscles, and have determined the effects of an endurance training program on these various parameters. Our results demonstrate that the intrinsic properties of muscular mitochondria, remain normal in heart transplant recipient, long after transplantation, either at the level of quantitative functional characteristics than at their adaptative mechanisms of regulation of cellular energy production and transfer. This study suggests that the muscular mitochondrial function and its adaptative mechanisms are not directly affected in vivo by clinical immunosuppressive treatment. Others non-mitochondrial actors such as the capillary network and some signaling pathways implicated in phenotypic muscular transition, should represent preferential targets of immunosuppressive drugs in peripheral muscle of heart transplant recipient
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Caiveau, Olivier. "Propriétés dynamiques et fonctionnelles des membranes des mitochondries de mutants d'Arabidopsis thaliana affectés dans les activités désaturases du reticulum endoplasmique." Paris 6, 2001. http://www.theses.fr/2001PA066403.

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Nait, Eldjoudi Amina. "Unraveling escape and metastasis mechanisms in triple negative breast cancer following chemotherapy treatment." Electronic Thesis or Diss., Université de Lille (2022-....), 2023. http://www.theses.fr/2023ULILS119.

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Le cancer du sein triple négatif (TNBC) est un sous-type particulièrement agressif du cancer du sein, traité principalement par chimiothérapie. Cependant, environ 50% des patients connaissent une rechute avec métastases dans les 3 à 5 ans suivant le traitement. Afin de mieux comprendre l'évasion post-chimiothérapie et la formation de métastases des cellules cancéreuses TNBC, nous avons établi des modèles de cellules TNBC en traitant les cellules SUM159-PT et MDA-MB-231 avec de l'épirubicine, du cyclophosphamide et du paclitaxel, simulant des protocoles cliniques. Nous nous sommes initialement concentrés sur l'adaptation mitochondriale de ces cellules persistantes. Les cellules MDA-MB-231 ont montré une sensibilité réduite à la chimiothérapie, associée à une phosphorylation oxydative accrue et à des intermédiaires du cycle de l'acide tricarboxylique modifiés. En revanche, les cellules SUM159-PT ont conservé leur sensibilité. Le ciblage du métabolisme mitochondrial du pyruvate avec le UK-5099 a resensibilisé les cellules persistantes MDA-MB-231 aux agents thérapeutiques. Les cellules persistantes ont montré une migration, une invasion et une survie accrues en culture en suspension, les cellules SUM159-PT présentant une adhésion accrue aux cellules endothéliales. Des études de xénogreffe in vivo ont confirmé ces observations, mettant l'accent sur une croissance cellulaire accrue et une colonisation métastatique dans des organes vitaux, en particulier le cerveau. Le tropisme accru pour le cerveau pourrait s'expliquer par le fait que les cellules TNBC persistantes présentaient une capacité accrue de traverser la barrière hémato-encéphalique, d'envahir le parenchyme cérébral et de croître dans une matrice 3D similaire au cerveau. Dans une deuxième phase de notre étude, nous avons étudié les mécanismes moléculaires facilitant la formation de métastases cérébrales de ces cellules persistantes. L'analyse protéomique a identifié des protéines surexprimées, notamment le COL1A1, fréquemment élevé chez les patients atteints de TNBC. Une augmentation de COL1A1 était corrélée à un mauvais pronostic et à une augmentation de la formation de métastase. L'inhibition de COL1A1 a réduit le potentiel métastatique à la fois in vitro et in vivo, soulignant son potentiel en tant que cible thérapeutique pour prévenir les métastases cérébrales après un traitement par chimiothérapie.L'ensemble de ces résultats offre un aperçu des mécanismes d'adaptation mis en place par les cellules cancéreuses en réponse à la chimiothérapie, et suggère que cibler le métabolisme du pyruvate mitochondrial pourrait contribuer à surmonter les adaptations mitochondriales des cellules de cancer du sein triple négatif. De plus, nos résultats mettent en lumière la manière dont une chimiothérapie combinée et séquentielle peut accroître le potentiel métastatique des cellules TNBC, en particulier vers le cerveau. Nous avons identifié la protéine COL1A1 comme un élément clé favorisant les différentes étapes de formation des métastases cérébrales dans les cellules TNBC résistantes à la chimiothérapie. Des recherches complémentaires sont nécessaires pour élucider les mécanismes détaillés de la surexpression de COL1A1.En utilisant le même schéma thérapeutique, nous avons mis en œuvre un traitement court de 48h, combiné et séquentiel pour évaluer les modifications protéomique précoces dans les vésicules extracellulaires libérées par les cellules TNBC persistantes. Avec cette approche, on a également exploré l'impact de la chimiothérapie sur les facteurs angiocrines des cellules endothéliales, suggérant le rôle du sécrétome induit par la chimiothérapie dans la facilitation des métastases post-chimiothérapie. Bien que ce volet de notre étude en soit à un stade préliminaire, les résultats encouragent à approfondir davantage l'investigation expérimentale
Triple negative breast cancer (TNBC) is a highly aggressive breast cancer subtype, primarily treated with chemotherapy. However, approximately 50% of patients experience relapse with metastasis within 3 to 5 years post-treatment. To gain insight into the post-chemotherapy escape and metastasis formation of TNBC cancer cells, we established TNBC cell models by treating SUM159-PT and MDA-MB-231 cells with epirubicin, cyclophosphamide, and paclitaxel. simulating clinical protocols. We initially focused on the mitochondrial adaptation of these chemo-persistent cells. MDA-MB-231 cells showed reduced chemosensitivity, associated with increased oxidative phosphorylation and altered tricarboxylic acid cycle intermediates. In contrast, SUM159-PT cells retained sensitivity. Targeting mitochondrial pyruvate metabolism with UK-5099 re-sensitized persistent cells to therapeutic agents, suggesting a potential strategy to overcome mitochondrial adaptation. Persistent cells exhibited increased migration, invasion, survival in suspension culture, with SUM159-PT cells displaying increased adhesion to endothelial cells. In vivo xenograft studies confirmed these observations, emphasizing increased cell growth and metastatic colonization in vital organs, particularly the brain. The enhanced trophism for brain could be explained by the fact that persistent TNBC cells exhibited increased abilities to transmigrate through BBB, to invade the brain parenchyma and to grow in a brain-like 3D matrix. In a second phase of our study, we investigated the molecular mechanisms facilitating brain metastasis of these persistent cells. proteomic analysis identified upregulated proteins, notably COL1A1, frequently elevated in TNBC patients. Increased COL1A1 correlated with poor prognosis and enhanced metastasis. Inhibition of COL1A1 reduced metastatic potential both in vitro and in vivo, highlighting its potential as a therapeutic target in preventing brain metastasis post chemotherapy treatment.Collectively, these findings provide insight into the adaptive mechanisms employed by cancer cells in response to chemotherapy, and suggest that targeting mitochondrial pyruvate metabolism may help to overcome the mitochondrial adaptations in TNBC cells. Furthermore, our data illuminate how combined and sequential chemotherapy may increase the metastatic potential of TNBC cells, particularly towards the brain. We have pinpointed COL1A1 as a key factor promoting various stages of brain metastasis formation in chemotherapy-resistant TNBC cells. Additional research is required to elucidate the detailed mechanisms behind COL1A1 overexpression.Using the identical drug regimen, we implemented a short, combined, and sequential treatment to replicate initial proteomic alterations in extracellular vesicles released by persistent TNBC cells. This approach also explored the impact of chemotherapy on angiocrine factors from endothelial cells, suggesting the role of the chemo-induced secretome in evading treatment and facilitating metastasis post-chemotherapy. Although this aspect of our study is currently in its early phases, the findings underscore the necessity for further experimental validation
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Singh, François. "Skeletal muscle toxicity and statins : role of mitochondrial adaptations." Thesis, Strasbourg, 2016. http://www.theses.fr/2016STRAJ050/document.

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Bien que les statines forment la classe d'hypolipidémiants la plus utilisée, une toxicité musculaire a été reportée, pouvant ainsi provoquer l’apparition d’une myopathie. Dans la première partie, nous avons montré chez l’Homme et l’animal que les statines inhibent directement la chaine respiratoire mitochondriale, et induisent la production de radicaux libres dérivés de l’oxygène (RLO), qui active les voies apoptotiques dans les muscles glycolytiques, alors que les muscles oxydatifs ne sont pas atteints. Nous avons ensuite montré in vitro que le stress réducteur peut engendrer une oxydation mitochondriale, pouvant conduire à une activation de la voie de biogenèse mitochondriale. De plus l’augmentation du contenu mitochondrial induite a permis de protéger les cellules contre l’apoptose induite par les statines. Enfin, nous avons montré in vivo que l’induction des voies de biogenèse mitochondriale est nécessaire à la tolérance des statines dans les muscles oxydatifs. En conclusion, le phénotype mitochondrial, tant au niveau quantitatif que qualitatif, semble être un facteur clé dans l’apparition de la myopathie aux statines
Although statins are the most prescribed class of lipid-lowering agents, adverse muscular toxicity has been reported, which can lead to the appearance of a myopathy. In the first part, we showed in Humans and animals that statins inhibit directly the mitochondrial respiratory chain, and induce the production of reactive oxygen species (ROS), that trigger apoptotic pathways in glycolytic skeletal muscles, whereas oxidative muscles are not impaired. We then showed in vitro that reductive stress can provoke mitochondrial oxidation, that could lead to an activation of mitochondrial biogenesis pathways. Moreover, the consequent increase in mitochondrial content enabled to protect cells against statin-induced apoptosis. Finally, we showed in vivo that the induction of mitochondrial biogenesis is necessary for statin tolerance in oxidative skeletal muscles. In conclusion, mitochondrial phenotype, both quantitatively and qualitatively, seems to be a key factor in the appearance of statin myopathy
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Schlagowski, Anna Isabel. "Etude des adaptations mitochondriales dans le muscle squelettique : importance de l'hormèse mitochondriale." Thesis, Strasbourg, 2014. http://www.theses.fr/2014STRAJ105/document.

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Les mécanismes impliqués dans les adaptations du phénotype métabolique musculaire au cours de l’exercice physique restent imparfaitement connus. Nous nous sommes intéressés au concept d’hormèse mitochondriale qui se définit comme un stress métabolique activant les voies de signalisation menant à une activation mitochondriale.En première partie, nous avons validé l’utilisation d’un nouveau système de mesure des échanges gazeux chez le rat au cours de différents exercices sur tapis roulant, et démontré que pour une vitesse de course sous maximale, un exercice en descente sollicite le système cardiovasculaire de façon modérée sans altérer la fonction mitochondriale musculaire, ni augmenter la production de radicaux libres oxygénés.En deuxième partie, nous avons montré qu’un découplage mitochondrial provoqué par un traitement des rats au 2,3-dinitrophénol (DNP) pendant 3 semaines engendre des adaptations métaboliques menant à l’augmentation de la masse mitochondriale du muscle squelettique. Ces animaux ont une capacité à l’exercice diminuée, malgré une augmentation de leur VO2max.Pour finir, nous avons montré qu’un préconditionnement par l’exercice protège la mitochondrie musculaire squelettique des effets délétères de l’ischémie-reperfusion. L’exercice semble activer le métabolisme via un phénomène d’hormèse mitochondriale permettant la protection musculaire. En conclusion, cette thèse nous montre d’une part l’importance de la mitochondrie (aspect quantitatif mais surtout qualitatif) en terme de limitation à l’exercice, et d’autre part nous suggère que l'optimisation du fonctionnement mitochondrial pourrait être une bonne garantie pour pouvoir lutter efficacement contre les stress, notamment oxydatifs, auxquels l'organisme est soumis en (quasi)permanence
The mechanisms regulating the metabolic phenotype adaptations in skeletal muscle during physical exercise is still unknown.We studied the mitochondrial hormesis phenomenon that could be defined as a metabolic stress activating the signaling pathways leading to a mitochondrial stimulation (mitochondrial biogenesis).In the first part, we validated the utilization of a new system determining the gas exchange in rat during a treadmill exhaustive exercise. We showed that a submaximal downhill exercise activate moderately the cardiovascular system, without mitochondrial functional impairments and without any augmentation of the systemic ROS production. In the second part, we showed that a mitochondrial uncoupling following a dinitrophenol treatment during 3 weeks in rats induced some metabolic adaptations leading to a higher mitochondrial mass in skeletal muscle. The exercise capacity of these animals is reduced whereas the maximal oxygen consumption is higher.In the last part, we showed that a preconditioning protocol with an acute exercise protected the skeletal muscle mitochondria from the deleterious effects of ischemia-reperfusion. This exercise seems to activate the muscular metabolism via a phenomenon of mitochondrial hormesis activation, allowing an efficient muscular protection.In conclusion, this thesis shows the importance of the mitochondria in terms of qualitative and quantitative aspects and shows the participation of this organelle in the exercise limitation. Moreover, these works suggest that the optimization of the mitochondrial function could be a good guarantee in order to efficiently fight against oxidative stress at the level of the whole organism
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Buchet-Poyau, Karine. "Cellules humaines dépourvues d'ADN mitochondrial : métabolisme adaptatif et utilisation dans l'étude génétique des pathologies mitochondriales." Lyon 1, 1999. http://www.theses.fr/1999LYO10192.

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Dans les cellules eucaryotes aerobies, l'energie provient essentiellement de l'atp synthetise par les phosphorylations oxydatives (oxphos) au niveau de l'atpase-atpsynthetase f0-f1. L'atp est alors exporte hors des mitochondries par le translocateur des nucleotides adenyliques (ant). Certaines sous-unites des complexes oxphos sont codees par l'adn mitochondrial (adnmt), les autres par l'adn nucleaire et importees dans les mitochondries par un mecanisme faisant intervenir le potentiel de membrane mitochondrial (pmm) etabli par les oxphos. Nous avons verifie que 2 lignees de cellules rho o humaines sont totalement depourvues d'adnmt, d'arn et de proteines codees par l'adnmt. Par contre, elles importent normalement des proteines d'origine nucleaire dans leurs mitochondries. Comment un pmm suffisant pour cette importation peut s'etablir dans les rho o en l'absence des oxphos ? nous avons montre que les rho o, depourvues des 2 sous-unites du facteur f0 de l'atpase-atpsynthetase codees par l'adnmt, ont un f1 assemble et fonctionnel pour hydrolyser de l'atp. De plus, 2 inhibiteurs specifiques de f1 (aurovertine) ou de l'ant (acide bongkrekique) reduisent la croissance et le pmm des rho o. Ainsi, la survie des rho o necessite un pmm suffisant maintenu par l'importation d'atp 4 cytosolique dans la mitochondrie par l'ant qui l'echange contre de l'adp 3 mitochondrial produit par l'atpase-f1. Nous avons egalement utilise les rho o pour determiner l'origine genetique de pathologies dues a un deficit d'un complexe oxphos. Les cellules de 3 patients atteints du syndrome de leigh avec deficit en cytochrome oxydase (cox) ont ete enucleees et fusionnees avec les rho o. L'activite cox etant restauree dans les cybrides, le deficit est localise sur l'adn nucleaire des patients. Par contre, la fusion a ete inutilisable pour determiner l'origine d'un deficit en complexe iii. En effet, le deficit est rapidement perdu dans les lymphocytes en culture suggerant un defaut heteroplasmique de l'adnmt.
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7

Butera, Gaia. "Mitochondrial adaptation in parvalbumin knockout muscle fibres." Doctoral thesis, Università degli studi di Padova, 2019. http://hdl.handle.net/11577/3422345.

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Mitochondrial Ca2+ homeostasis plays a fundamental role in the regulation of several biological processes, ranging from the regulation of ATP production to the control of cell death. Recent studies have identified the multimolecular complex responsible for Ca2+ entry into mitochondria: the mitochondrial calcium uniporter (MCU) complex [1]. It is widely accepted that mitochondria actively participate in the regulation of cellular Ca2+ homeostasis by dictating the spatio-temporal properties of [Ca2+]cyt rises [2]. Mitochondrial calcium uptake, in specific cells, contributes to regulate cellular Ca2+ homeostasis acting as high-capacity fixed buffer, sequestering large amounts of Ca2+ from a subcellular domain[2]. Furthermore, one of the most important roles of mitochondrial Ca2+ uptake is the mitochondrial Ca2+-dependent control of the rate of mitochondrial adenosine triphosphate (ATP) production, the main fuel for sustaining cellular functions [3], [4]. This general picture is particularly relevant in skeletal muscle, a tissue where mitochondria produce most of the ATP required to sustain muscle contraction [3], [5]. It is thus not surprising that skeletal muscle mitochondria display the highest mitochondrial Ca2+ transients, as demonstrated by the measurement of the MCU current by patch-clamp from IMM-derived mitoplasts from different tissues [6]. Moreover, pivotal findings have highlighted the role of mitochondria as key players in the dynamic regulation of crucial signalling pathways in skeletal muscle [7], [8], involved not only in muscle contraction but also in skeletal muscle homeostasis [9], [10]. However, whether skeletal muscle mitochondria act also as a possible high capacity Ca2+ buffer remains a fundamental question on muscle physiology and diseases. Our research investigated the regulatory processes that modulate mitochondrial Ca2+ signalling in skeletal muscle. In detail, to understand the impact of changes in cytosolic Ca2+ concentrations ([Ca2+]cyt) on mitochondrial Ca2+ uptake and muscle physiology, we explored a condition where intra-fiber Ca2+ kinetics have been profoundly altered by removing parvalbumin (PV), one of the crucial cytosolic Ca2+ buffers in skeletal muscle, specifically expressed in fast twitch muscle fibers [11], [12]. To this end, as study tool, we used a PV knockout (KO) mouse model obtained from the laboratory of Prof. Beat Schwaller (Dept. of Medicine, University of Fribourg, Switzerland) [13]. PV plays an important role in skeletal muscle, acting as a temporary Ca2+ buffer (e.g. increasing the relaxation rate of fast twitch muscle contraction) [14]. To investigate the physiological role of PV in muscle fibers and in Ca2+ homeostasis, we investigated cytosolic and mitochondrial Ca2+ transients in PV KO mice compared. We observed that basal [Ca2+]cyt was not affected in PV knockout fibers, but kinetics of Ca2+ transients and Ca2+ clearance were altered. In detail, consistently with the role of PV in buffering cytosolic Ca2+, the time-to-peak and the half-relaxation time was increased in PV KO FDB fibers. Unexpectedly, however, under tetanic stimulation, PV KO FDB muscle fibers showed a decrease in [Ca2+]cyt. To explain this result we asked whether the lack of PV could induce rearrangements of one of the two main Ca2+ stores, the sarcoplasmic reticulum (SR) and mitochondria. SR Ca2+ measurements demonstrated that lack of PV increases SR Ca2+ release during stimulation. Therefore, we concluded that SR is not causative of the effect of PV removal on cytosolic Ca2+ transients. Consistently, we found no difference in the mRNA levels of RyR1, the main Ca2+ releasing channel in muscle, and on the expression of two different isoforms of SERCA in PV KO muscles compared to WT. We then focused our attention on mitochondrial Ca2+ homeostasis. The data obtained demonstrated that the lack of PV induces an increase of mitochondrial Ca2+ uptake and this is accompanied by the induction of the expression of MCU complex components, the channel responsible for Ca2+ entry in mitochondria [1], [2], [15], [16]. In addition, electron microscopy analysis demonstrated that the volume of PV KO mitochondria was doubled compared to WT with an increase of mitochondria associated to the Ca2+ release units (CRUs), suggesting a tight connection of PV expression with mitochondrial morphology and function in muscle cells. Furthermore, to further prove that mitochondria are responsible for cytosolic Ca2+ buffering in fibers lacking PV, we silenced MCU on WT and PV KO FDB fibers and we measured [Ca2+]cyt.. In WT animals, [Ca2+]cyt was not affected by the absence of MCU, while MCU silencing in PV KO fibers resulted in a significant higher [Ca2+]cyt, reinforcing the hypothesis that, while in WT animals mitochondria do not significantly buffer [Ca2+]cyt, mitochondria of fibers lacking PV adapt to buffer [Ca2+]cyt increases. Moreover, since PV is one of the most downregulated “atrogenes”, the genes commonly up- and down-regulated during both disuse and systemic types of atrophy [17], [18] and that mitochondrial Ca2+ controls skeletal muscle trophism [10], the role of PV in the regulation of muscle mass was investigated through denervation experiments. In PV KO muscles, loss of muscle mass caused by denervation is reduced compared to WT fibers, demonstrating that the lack of PV can partially protect muscles from denervation-induced atrophy. Since the effect of PV ablation on denervated muscle was modest and the effect on innervated muscles was negligible, we decided to perform PV acute silencing and overexpression in adult WT tibialis anterior (TA) muscles and we monitored fiber size. We demonstrated that the acute modulation of PV protein controls skeletal muscle size. In detail, we observed an increase of fiber size in PV silenced muscles and coherently, PV overexpressing muscles displayed an atrophic phenotype. Since the regulation of muscle size involves a precise transcriptional program [18], [19], we focused our attention on PGC-1α4, a splicing variant of the PGC-1α gene, that plays a key role in triggering muscle hypertrophy as adaptive response to exercise [20]. Intriguingly, we found an up-regulation of PGC-1α4 mRNA in PV KO skeletal muscles, suggesting the activation of this hypertrophic pathway. Of note, our data are in accordance with previous studies showing that mitochondrial Ca2+ positively regulates skeletal muscle mass by impinging also on PGC-1α4 pathway [10]. Our results show that the lack of PV in skeletal muscle leads to morphological and functional adaptations of mitochondria. In particular, mitochondria of fibers lacking PV, either constitutively or transiently, adapt to take up more Ca2+ to control [Ca2+]cyt increases. Furthermore, we demonstrated that the absence of PV partially counteracts denervation atrophy by triggering the expression of PGC-1α4. Our hypothesis is that PV ablation, leading to an increase of mitochondrial Ca2+ uptake, activates mitochondrial Ca2+-dependent pathways to control skeletal muscle trophism.
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Salle, Agnès. "Métabolisme énergétique chez l'obèse et le diabetique de type 2." Angers, 2006. http://www.theses.fr/2006ANGE0054.

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L'évolution pondérale des diabétiques de type 2 (DT2) est particulière avec une propension à prendre du poids sous insuline, et à l'inverse des difficulés à en perdre lors des programmes de réduction pondérale. Nos résultats montrent qu'après un an de traitement par insuline la prise de poids est faite préférentiellement de masse maigre et suggèrent qu'elle n'augmente pas le risque vasculaire. Nos résultats montrent également qu'au stade précoce de leur maladie, les DT2 peuvent perdre la même quantité de poids que les obèses et que dans les deux cas il n'a pas d'adaptation du métabolisme énergétique corps entier ou mitochondrial pouvant expliquer le plateau pondéral observé à partir du cinquième mois. Il n'y a pas non plus d'adaptation particulière du métabolisme énergétique chez les DT2, leur métabolisme de base n'étant pas différent de celui des obèses à poids stable comme après perte de poids et l'insulinorésistance n'est pas un déterminant du métabolisme énergétique
Weight change in type 2 diabetic patients (T2D) is distinctive with an inclination towards weight gain with insulin, and conversely a difficulty in weight loss in weight reduction programmes. Our results show that after one year of insulin treatment, resultant weight gain is composed primarly of fat-free mass and it appears not to incrase cardivascular risk. Our results also show that in the early stage of their disease, T2D lose the same amount of weight as obese nondiabetic patients and that in both cases there is non whole body or mitochondrial energy metabolism adaptation that can explain the stabilisation of weight observed from the 5th month onwards. Furthermore, there is no specific adaptation of energy metabolism in T2D as their basal metabolism is not any different to that of obese nondiabetic patients or after weight loss. Insulin resistance is not a determinant of energy metabolism
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Bigger, Brian William. "Adaptation of the mitochondrial genome as a vehicle for gene delivery." Thesis, Imperial College London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325568.

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Bertaux, Audrey. "Influence du métabolisme mitochondrial dans l'hématopoïèse : Analyse de la réponse adaptative des cellules de la moelle osseuse et des thymocytes au dysfonctionnement de l’OXPHOS." Thesis, Sorbonne université, 2018. http://www.theses.fr/2018SORUS040/document.

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Les mitochondries sont des organelles qui jouent un rôle clé dans le métabolisme cellulaire en centralisant la production d'ATP à partir de nombreux substrats via la phosphorylation oxydative (OXPHOS). Les réactions enzymatiques impliquées dans ce processus régulent la prolifération, la différenciation, l'activation et l'auto renouvellement cellulaire. Le but de mon travail a été d'identifier le rôle de l'OXPHOS dans l'hématopoïèse et les mécanismes d'adaptation métabolique des cellules sanguines de la moelle, des lymphocytes B et des thymocytes à la dysfonction mitochondriale. L'atout majeur de cette étude est la génération de deux modèles murins déficients pour les protéines mitochondriales AIF ou NDUFS4 dans le système hématopoïétique. Nous avons observé que l'absence de ces protéines entraine des dysfonctions de l'OXPHOS sévère (AIF KO) ou modérée (NDUFS4 KO), entrainant des anomalies dans le développement hématopoïétique. Dans les deux modèles, en réponse au stress métabolique induit par la dysfonction de l'OXPHOS, les cellules de moelle activent la glycolyse anaérobie et la biogenèse mitochondriale tandis que les thymocytes favorisent l'assimilation et la dégradation des acides gras. Cette étude multiparamétrique, incluant des approches in vivo, ex vivo et in vitro, souligne l'importance de l'OXPHOS et du métabolisme mitochondrial dans le développement hématopoïétique
By integrating different biochemical pathways and generating energy in form of ATP, through the electron transfer associated to oxidative phosphorylation (OXPHOS), mitochondria play a key role in cellular metabolism. In the hematopoietic cells, the mitochondrial metabolism appears implicated in proliferation, differentiation, activation and self-renewal regulation. In this context, the aim of my PhD work was to unravel the response of bone marrow (BM) cells, B-cells and thymocytes to OXPHOS dysfunction. To do that, we have developed two original hematopoietic cell-specific murine models deficient in the mitochondrial proteins AIF or NDUFS4. Severe (AIF KO) or moderate (NDUFS4 KO) OXPHOS dysfunction leads to pleiotropic consequences on hematopoietic development, including pancytopenia, BM aplasia, alterations in the development of the B-cell and erythroid lineages and T-cell developmental blockade at the immature stage. Strikingly, in response to OXPHOS dysfunction, BM cells stimulate anaerobic glycolysis and mitochondrial biogenesis, whereas thymocytes favor the assimilation and degradation of fatty acids. Overall my work, which included in vivo, ex vivo and in vitro approaches, underlines the relevance of OXPHOS and mitochondrial metabolism in the development of the hematopoietic cells
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Books on the topic "Adaptation mitochondriale"

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MacPherson, Laura Lynn. Adaptations of skeletal muscle pyruvate dehydrogenase kinase in response to food-restriction in mitochondrial subpopulations. St. Catharines, Ont: Brock University, Faculty of Applied Health Sciences, 2007.

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Sukhamay, Lahiri, Cherniack Neil S, Fitzgerald Robert S. 1931-, American Physiological Society (1887- ), and Federation of American Societies for Experimental Biology., eds. Response and adaptation to hypoxia: Organ to organelle. New York: Published for the American Physiological Society by Oxford University Press, 1991.

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Fitzgerald, Robert S., Neil S. Cherniak, and Sukhamay Lahiri. Response and Adaptation to Hypoxia: Organ to Organelle. Springer, 2013.

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Hill, Geoffrey E. Mitonuclear Ecology. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198818250.001.0001.

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Eukaryotes were born of a chimeric union of two prokaryotes. The legacy of this fusion is organisms with both a nuclear and mitochondrial genome that must work in a coordinated fashion to enable cellular respiration. The coexistence of two genomes in a single organism requires tight coadaptation to enable function. The need for coadaptation, the challenge of co-transmission, and the possibility of genomic conflict between mitochondrial and nuclear genes have profound consequences for the ecology and evolution of eukaryotic life. This book defines mitonuclear ecology as an emerging field that reassesses core concepts in evolutionary ecology in light of the necessity of mitonuclear coadaptation. I discuss and summarize research that tests new mitonuclear-based theories for the evolution of sex, two sexes, senescence, a sequestered germ line, speciation, sexual selection, and adaptation. The ideas presented in this book represent a paradigm shift for evolutionary ecology. Through the twentieth century, mitochondrial genomes were dismissed as unimportant to the evolution of complex life because variation within mitochondrial genomes was proposed to be functionally neutral. These conceptions about mitochondrial genomes and mitonuclear genomic interactions have been changing rapidly, and a growing literature in top journals is making it increasingly clear that the interactions of the mitochondrial and nuclear genomes over the past 2 billion years have played a major role in shaping the evolution of eukaryotes. These new hypotheses for the evolution of quintessential characteristics of complex life hold the potential to fundamentally reshape the field of evolutionary ecology and to inform the emerging fields of mitochondrial medicine and mitochondrial-based reproductive therapies.
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(Editor), Sukhamay Lahiri, Neil S. Cherniak (Editor), and Robert S. Fitzgerald (Editor), eds. Response and Adaptation to Hypoxia: Organ to Organelle (Clinical Physiology Series). An American Physiological Society Book, 1991.

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Dodds, Chris, Chandra M. Kumar, and Frédérique Servin. Pathophysiological changes of ageing and their relevance to anaesthesia. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198735571.003.0002.

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The molecular basis of ageing is reviewed. This includes the concept of a summation of DNA damage over a lifetime causing genome instability. Epigenetic alterations, telomeric shortening, and the possibility of their modification are discussed. Oxidative and mitochondrial DNA damage and the resulting dysfunction leading to senescence are briefly described. Systemic problems and resultant behavioural adaptation may mask the decline in functional reserve and cause some of the difficulties in identifying its presence in ill elderly patients. Specific organ system changes are then described in some detail. These include the major concerns with the cardiovascular, respiratory, renal, hepatic, neurologic, endocrine, and musculoskeletal systems. The effect of ageing on the special senses of vision and hearing are covered, with emphasis on issues of informed consent.
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Book chapters on the topic "Adaptation mitochondriale"

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Grip, Jonathan, Nicolas Tardif, and Olav Rooyackers. "Mitochondrial Adaptation and Hibernation." In The Stress Response of Critical Illness: Metabolic and Hormonal Aspects, 27–43. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-27687-8_4.

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Lombard, David B., Daniel X. Tishkoff, and Jianjun Bao. "Mitochondrial Sirtuins in the Regulation of Mitochondrial Activity and Metabolic Adaptation." In Histone Deacetylases: the Biology and Clinical Implication, 163–88. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-21631-2_8.

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Landau, Alejandra, Franco Lencina, María Elizabeth Petterson, María Gabriela Pacheco, Susana Costoya, Vanina Brizuela, and Alberto Prina. "The barley chloroplast mutator (cpm) mutant, an extraordinary source of plastome variability." In Mutation breeding, genetic diversity and crop adaptation to climate change, 271–79. Wallingford: CABI, 2021. http://dx.doi.org/10.1079/9781789249095.0027.

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Abstract The plastome is usually considered a highly conserved genome. Compared with the nuclear genome, it is small and has different genetic rules. Through different molecular methods (TILLING, candidate gene sequencing, amplicon massive sequencing and plastome re-sequencing) applied to barley chloroplast mutator (cpm) seedlings, we detected more than 60 polymorphisms affecting a wide variety of plastid genes and several intergenic regions. The genes affected belonged mostly to the plastid genetic machinery and the photosynthetic apparatus, but there were also genes like matK, whose functions are so far not clearly established. Among the isolated mutants, we found the first infA gene mutant in higher plants, two mutants in ycf3 locus and the first psbA gene mutant in barley. The latter is used in breeding barley cultivars where PSII is tolerant to toxic herbicides. Most of the molecular changes were substitutions, and small indels located in microsatellites. However, particular combinations of polymorphisms observed in the rpl23 gene and pseudogene suggest that, besides an increased rate of mutations, an augmented rate of illegitimate recombination also occurred. Although a few substitutions were observed in the mitochondria of cpm plants, we have not yet determined the implications of the cpm for mitochondrial stability. The spectrum of plastome polymorphisms highly suggests that the cpm gene is involved in plastid DNA repair, more precisely taking part in the mismatch repair system. All results show that the cpm mutant is an extraordinary source of plastome variability for plant research and/or plant breeding. This mutant also provides an interesting experimental system in which to investigate the mechanisms responsible for maintaining plastid stability.
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Hedges, Christopher P., and Troy L. Merry. "Mitochondrial Redox Regulation in Adaptation to Exercise." In Oxidative Eustress in Exercise Physiology, 59–70. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003051619-5.

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Weibel, Ewald R., and Hans Hoppeler. "Respiratory System Adaptation to Hypoxia: Lung to Mitochondria." In Response and Adaptation to Hypoxia, 3–13. New York, NY: Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4614-7574-3_1.

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Seppet, Enn, Ehte Orlova, Teet Seene, and Frank N. Gellerich. "Adaptation of Cardiac and Skeletal Muscle Mitochondria to Endurance Training: Implications for Cardiac Protection." In Cardiac Adaptations, 375–402. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5203-4_20.

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Wilson, David F., and William L. Rumsey. "Factors Affecting Adaptation of the Mitochondrial Enzyme Content to Cellular Needs." In Response and Adaptation to Hypoxia, 14–24. New York, NY: Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4614-7574-3_2.

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Jones, Dean P., Tak Yee Aw, Changli Bai, and A. H. Sillau. "Regulation of Mitochondrial Distribution: An Adaptive Response to Changes in Oxygen Supply." In Response and Adaptation to Hypoxia, 25–35. New York, NY: Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4614-7574-3_3.

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Hoppeler, H. "The Range of Mitochondrial Adaptation in Muscle Fibers." In The Dynamic State of Muscle Fibers, edited by Dirk Pette, 567–86. Berlin, Boston: De Gruyter, 1990. http://dx.doi.org/10.1515/9783110884784-045.

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Castilho, Roger F., André R. Meinicke, Anibal E. Vercesi, and Marcelo Hermes-Lima. "Role of Fe(III) in Fe(II)citrate-mediated peroxidation of mitochondrial membrane lipids." In Stress Adaptation, Prophylaxis and Treatment, 163–68. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-5097-6_20.

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Conference papers on the topic "Adaptation mitochondriale"

1

Petrenko, V. S., V. V. Vrublevskaya, M. A. Zhmurina, Yu Yu Skarga, and O. S. Morenkov. "ADAPTATION OF THE CHAPERONE MACHINE OF HUMAN FIBROSARCOMA HT1080 CELLS TO THE LOSS OF HSP90Α AS A RESULT OF THE KNOCKOUT OF THE HSP90AA1 GENE." In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-356.

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Knockout of the HSP90AA1 gene encoding Hsp90α in HT1080 human fibrosarcoma cells was accompanied by adaptation of the cellular chaperone machine to Hsp90α loss. Adaptation included increased expression of Hsp90β, key Hsp90 co-chaperones, chaperones and co-chaperones of the Hsp70/Hsp40 complex, components of the TRiC/CCT complex, prefoldins, prefoldin-like PFDL, R2TP, and R2SP chaperone complexes, as well as key mitochondrial chaperones and chaperonins.
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Шунькина, Дарья Александровна, Александра Андреевна Комар, Мария Александровна Вульф, Елена Витальевна Кириенкова, and Лариса Сергеевна Литвинова. "PLASMA IL-6 IS ASSOCIATED WITH DECREASED TFAM GENE EXPRESSION IN THE LIVER IN OBESE PATIENTS WITH TYPE 2 DIABETES." In Фундаментальные и прикладные исследования. Актуальные проблемы и достижения: сборник избранных статей Всероссийской (национальной) научной конференции (Санкт-Петербург, Декабрь 2021). Crossref, 2022. http://dx.doi.org/10.37539/fipi323.2021.56.58.002.

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Биогенез митохондрий регулируется организованной индукции нескольких транскрипционных факторов. Утрата митохондриальной адаптации способствует сахарному диабету 2 типа. Высокий уровень IL-6 в плазме крови пациентов с ожирением взаимосвязан со снижением экспрессии гена TFAM в биоптатах печени. Уровень экспрессии гена TFAM в биоптатах печени у больных с СД 2 типа снижался относительно контрольной группы. Mitochondrial biogenesis is regulated by the organized induction of several transcription factors. Loss of mitochondrial adaptation contributes to type 2 diabetes. A high level of IL-6 in the blood plasma of obese patients is associated with a decrease in TFAM gene expression in liver biopsies. The expression level of the TFAM gene in liver biopsies of patients with type 2 diabetes decreased relative to the control group.
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Zhou, H., Y. Shi, X. Zhang, and Y. Ke. "Mitochondrial Adaptations in Lipid Metabolism in Lung Metastases." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a4930.

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Grieco, Joseph P., Stephanie Edwards, Mitchell Allen, Yao Wang, Justin Perry, Yipei Song, Nathan Swami, David Brown, and Eva Schmelz. "Abstract 805: Adaptation of mitochondrial organization to aggregation in serous ovarian cancer." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-805.

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Grieco, Joseph P., Stephanie Edwards, Mitchell Allen, Yao Wang, Justin Perry, Yipei Song, Nathan Swami, David Brown, and Eva Schmelz. "Abstract 805: Adaptation of mitochondrial organization to aggregation in serous ovarian cancer." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-805.

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Grabelnych, O. I., T. P. Pobezhimova, N. S. Zabanova, O. A. Borovik, and V. K. Voinikov. "THE PLANT MITOCHONDRIA UNDER STRESS AND ADAPTATION TO HYPO- AND HYPERTHERMIA." In The Second All-Russian Scientific Conference with international participation "Regulation Mechanisms of Eukariotic Cell Organelle Functions". SIPPB SB RAS, 2018. http://dx.doi.org/10.31255/978-5-94797-318-1-27-29.

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Marcus, Jeffrey M. "Mitochondrial phylogenomics and high-altitude adaptation in the New World buckeye butterflies (Genus Junonia)." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.114062.

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"Adaptation of the CRISPR/Cas9 system for targeted manipulations of the human mitochondrial genome." In SYSTEMS BIOLOGY AND BIOINFORMATICS. Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, 2019. http://dx.doi.org/10.18699/sbb-2019-43.

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Giulietti, Kevin, Guillaume Lavisse, Aurelie Charazac, Stephan Clavel, Frederic Bost, and Xavier Descombes. "An Adaptative Threshold Operator Taking Shape into Account: Application to Mitochondrial Network Segmentation." In 2019 IEEE 16th International Symposium on Biomedical Imaging (ISBI). IEEE, 2019. http://dx.doi.org/10.1109/isbi.2019.8759501.

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Yashin, K. E., N. A. Sokolov, Evgeni Pavlovich Vasiliev, and A. A. Getmanskaya. "Dataset Extension for Neural Networks Training for the Mitochondrial Segmentation Problem of the Brain Electron Microscopy." In 33rd International Conference on Computer Graphics and Vision. Keldysh Institute of Applied Mathematics, 2023. http://dx.doi.org/10.20948/graphicon-2023-654-662.

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This paper presents the adaptation of a diffusion neural network to generate a labeled synthetic dataset of electron microscopy of the brain. A model was trained can generate images and markup for them at the same time, which is an undoubted advantage of the chosen approach. Using the trained model, a set of labeled images was generated. The synthetic images are visually very similar to the original ones, the FID similarity metric between the synthetic and original datasets is 27.1. A simplified U-Net segmentation model trained on a mixed data set (original data + synthetic data) obtained a Dice score of 0.856 versus 0.858 on the original training set. Despite the good quality of synthetic data, their use in training the segmentation network does not improve the segmentation results.
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Reports on the topic "Adaptation mitochondriale"

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Schuster, Gadi, and David Stern. Integration of phosphorus and chloroplast mRNA metabolism through regulated ribonucleases. United States Department of Agriculture, August 2008. http://dx.doi.org/10.32747/2008.7695859.bard.

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New potential for engineering chloroplasts to express novel traits has stimulated research into relevant techniques and genetic processes, including plastid transformation and gene regulation. This proposal continued our long time BARD-funded collaboration research into mechanisms that influence chloroplast RNA accumulation, and thus gene expression. Previous work on cpRNA catabolism has elucidated a pathway initiated by endonucleolytic cleavage, followed by polyadenylation and exonucleolytic degradation. A major player in this process is the nucleus-encoded exoribonuclease/polymerasepolynucleotidephoshorylase (PNPase). Biochemical characterization of PNPase has revealed a modular structure that controls its RNA synthesis and degradation activities, which in turn are responsive to the phosphate (P) concentration. However, the in vivo roles and regulation of these opposing activities are poorly understood. The objectives of this project were to define how PNPase is controlled by P and nucleotides, using in vitro assays; To make use of both null and site-directed mutations in the PNPgene to study why PNPase appears to be required for photosynthesis; and to analyze plants defective in P sensing for effects on chloroplast gene expression, to address one aspect of how adaptation is integrated throughout the organism. Our new data show that P deprivation reduces cpRNA decay rates in vivo in a PNPasedependent manner, suggesting that PNPase is part of an organismal P limitation response chain that includes the chloroplast. As an essential component of macromolecules, P availability often limits plant growth, and particularly impacts photosynthesis. Although plants have evolved sophisticated scavenging mechanisms these have yet to be exploited, hence P is the most important fertilizer input for crop plants. cpRNA metabolism was found to be regulated by P concentrations through a global sensing pathway in which PNPase is a central player. In addition several additional discoveries were revealed during the course of this research program. The human mitochondria PNPase was explored and a possible role in maintaining mitochondria homeostasis was outlined. As polyadenylation was found to be a common mechanism that is present in almost all organisms, the few examples of organisms that metabolize RNA with no polyadenylation were analyzed and described. Our experiment shaded new insights into how nutrient stress signals affect yield by influencing photosynthesis and other chloroplast processes, suggesting strategies for improving agriculturally-important plants or plants with novel introduced traits. Our studies illuminated the poorly understood linkage of chloroplast gene expression to environmental influences other than light quality and quantity. Finely, our finding significantly advanced the knowledge about polyadenylation of RNA, the evolution of this process and its function in different organisms including bacteria, archaea, chloroplasts, mitochondria and the eukaryotic cell. These new insights into chloroplast gene regulation will ultimately support plant improvement for agriculture
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