Relevant bibliographies by topics / Mice Mitochondria

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Mice Mitochondria'

Author: Grafiati
Published: 4 June 2021
Last updated: 8 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Mice Mitochondria.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Mice Mitochondria"

1

Rossi, Ann E., Simona Boncompagni, Lan Wei, Feliciano Protasi, and Robert T. Dirksen. "Differential impact of mitochondrial positioning on mitochondrial Ca2+ uptake and Ca2+ spark suppression in skeletal muscle." American Journal of Physiology-Cell Physiology 301, no. 5 (November 2011): C1128—C1139. http://dx.doi.org/10.1152/ajpcell.00194.2011.

Full text
Abstract:
Muscle contraction requires ATP and Ca2+ and, thus, is under direct control of mitochondria and the sarcoplasmic reticulum. During postnatal skeletal muscle maturation, the mitochondrial network exhibits a shift from a longitudinal (“longitudinal mitochondria”) to a mostly transversal orientation as a result of a progressive increase in mitochondrial association with Ca2+ release units (CRUs) or triads (“triadic mitochondria”). To determine the physiological implications of this shift in mitochondrial disposition, we used confocal microscopy to monitor activity-dependent changes in myoplasmic (fluo 4) and mitochondrial (rhod 2) Ca2+ in single flexor digitorum brevis (FDB) fibers from 1- to 4-mo-old mice. A robust and sustained Ca2+ accumulation in triadic mitochondria was triggered by repetitive tetanic stimulation (500 ms, 100 Hz, every 2.5 s) in FDB fibers from 4-mo-old mice. Specifically, mitochondrial rhod 2 fluorescence increased 272 ± 39% after a single tetanus and 412 ± 45% after five tetani and decayed slowly over 10 min following the final tetanus. Similar results were observed in fibers expressing mitochondrial pericam, a mitochondrial-targeted ratiometric Ca2+ indicator. Interestingly, sustained mitochondrial Ca2+ uptake following repetitive tetanic stimulation was similar for triadic and longitudinal mitochondria in FDB fibers from 1-mo-old mice, and both mitochondrial populations were found by electron microscopy to be continuous and structurally tethered to the sarcoplasmic reticulum. Conversely, the frequency of osmotic shock-induced Ca2+ sparks per CRU density decreased threefold (from 3.6 ± 0.2 to 1.2 ± 0.1 events·CRU−1·min−1·100 μm−2) during postnatal development in direct linear correspondence ( r2 = 0.95) to an increase in mitochondrion-CRU pairing. Together, these results indicate that mitochondrion-CRU association promotes Ca2+ spark suppression but does not significantly impact mitochondrial Ca2+ uptake.
APA, Harvard, Vancouver, ISO, and other styles
2

Williams, Jessica A., Hong-Min Ni, Yifeng Ding, and Wen-Xing Ding. "Parkin regulates mitophagy and mitochondrial function to protect against alcohol-induced liver injury and steatosis in mice." American Journal of Physiology-Gastrointestinal and Liver Physiology 309, no. 5 (September 1, 2015): G324—G340. http://dx.doi.org/10.1152/ajpgi.00108.2015.

Full text
Abstract:
Alcoholic liver disease claims two million lives per year. We previously reported that autophagy protected against alcohol-induced liver injury and steatosis by removing damaged mitochondria. However, the mechanisms for removal of these mitochondria are unknown. Parkin is an evolutionarily conserved E3 ligase that is recruited to damaged mitochondria to initiate ubiquitination of mitochondrial outer membrane proteins and subsequent mitochondrial degradation by mitophagy. In addition to its role in mitophagy, Parkin has been shown to have other roles in maintaining mitochondrial function. We investigated whether Parkin protected against alcohol-induced liver injury and steatosis using wild-type (WT) and Parkin knockout (KO) mice treated with alcohol by the acute-binge and Gao-binge (chronic plus acute-binge) models. We found that Parkin protected against liver injury in both alcohol models, likely because of Parkin's role in maintaining a population of healthy mitochondria. Alcohol caused greater mitochondrial damage and oxidative stress in Parkin KO livers compared with WT livers. After alcohol treatment, Parkin KO mice had severely swollen and damaged mitochondria that lacked cristae, which were not seen in WT mice. Furthermore, Parkin KO mice had decreased mitophagy, β-oxidation, mitochondrial respiration, and cytochrome c oxidase activity after acute alcohol treatment compared with WT mice. Interestingly, liver mitochondria seemed able to adapt to alcohol treatment, but Parkin KO mouse liver mitochondria had less capacity to adapt to Gao-binge treatment compared with WT mouse liver mitochondria. Overall, our findings indicate that Parkin is an important mediator of protection against alcohol-induced mitochondrial damage, steatosis, and liver injury.
APA, Harvard, Vancouver, ISO, and other styles
3

King, Adrienne L., Telisha M. Swain, Zhengkuan Mao, Uduak S. Udoh, Claudia R. Oliva, Angela M. Betancourt, Corrine E. Griguer, David R. Crowe, Mathieu Lesort, and Shannon M. Bailey. "Involvement of the mitochondrial permeability transition pore in chronic ethanol-mediated liver injury in mice." American Journal of Physiology-Gastrointestinal and Liver Physiology 306, no. 4 (February 15, 2014): G265—G277. http://dx.doi.org/10.1152/ajpgi.00278.2013.

Full text
Abstract:
Chronic ethanol consumption increases sensitivity of the mitochondrial permeability transition (MPT) pore induction in liver. Ca2+ promotes MPT pore opening, and genetic ablation of cyclophilin D (CypD) increases the Ca2+ threshold for the MPT. We used wild-type (WT) and CypD-null (CypD−/−) mice fed a control or an ethanol-containing diet to investigate the role of the MPT in ethanol-mediated liver injury. Ca2+-mediated induction of the MPT and mitochondrial respiration were measured in isolated liver mitochondria. Steatosis was present in WT and CypD−/− mice fed ethanol and accompanied by increased terminal deoxynucleotidyl transferase dUTP-mediated nick-end label-positive nuclei. Autophagy was increased in ethanol-fed WT mice compared with ethanol-fed CypD−/− mice, as reflected by an increase in the ratio of microtubule protein 1 light chain 3B II to microtubule protein 1 light chain 3B I. Higher levels of p62 were measured in CypD−/− than WT mice. Ethanol decreased mitochondrial respiratory control ratios and select complex activities in WT and CypD−/− mice. Ethanol also increased CypD protein in liver of WT mice. Mitochondria from control- and ethanol-fed WT mice were more sensitive to Ca2+-mediated MPT pore induction than mitochondria from their CypD−/− counterparts. Mitochondria from ethanol-fed CypD−/− mice were also more sensitive to Ca2+-induced swelling than mitochondria from control-fed CypD−/− mice but were less sensitive than mitochondria from ethanol-fed WT mice. In summary, CypD deficiency was associated with impaired autophagy and did not prevent ethanol-mediated steatosis. Furthermore, increased MPT sensitivity was observed in mitochondria from ethanol-fed WT and CypD−/− mice. We conclude that chronic ethanol consumption likely lowers the threshold for CypD-regulated and -independent characteristics of the ethanol-mediated MPT pore in liver mitochondria.
APA, Harvard, Vancouver, ISO, and other styles
4

Saleem, Ayesha, Sobia Iqbal, Yuan Zhang, and David A. Hood. "Effect of p53 on mitochondrial morphology, import, and assembly in skeletal muscle." American Journal of Physiology-Cell Physiology 308, no. 4 (February 15, 2015): C319—C329. http://dx.doi.org/10.1152/ajpcell.00253.2014.

Full text
Abstract:
The purpose of this study was to investigate whether p53 regulates mitochondrial function via changes in mitochondrial protein import, complex IV (COX) assembly, or the expression of key proteins involved in mitochondrial dynamics and degradation. Mitochondria from p53 KO mice displayed ultra-structural alterations and were more punctate in appearance. This was accompanied by protein-specific alterations in fission, fusion, and mitophagy-related proteins. However, matrix-destined protein import into subsarcolemmal or intermyofibrillar mitochondria was unaffected in the absence of p53, despite mitochondrial subfraction-specific reductions in Tom20, Tim23, mtHsp70, and mtHsp60 in the knockout (KO) mitochondria. Complex IV activity in isolated mitochondria was also unchanged in KO mice, but two-dimensional blue native-PAGE revealed a reduction in the assembly of complex IV within the IMF fractions from KO mice in tandem with lower levels of the assembly protein Surf1. This observed defect in complex IV assembly may facilitate the previously documented impairment in mitochondrial function in p53 KO mice. We suspect that these morphological and functional impairments in mitochondria drive a decreased reliance on mitochondrial respiration as a means of energy production in skeletal muscle in the absence of p53.
APA, Harvard, Vancouver, ISO, and other styles
5

Eismann, Thorsten, Nadine Huber, Thomas Shin, Satoshi Kuboki, Elizabeth Galloway, Michael Wyder, Michael J. Edwards, et al. "Peroxiredoxin-6 protects against mitochondrial dysfunction and liver injury during ischemia-reperfusion in mice." American Journal of Physiology-Gastrointestinal and Liver Physiology 296, no. 2 (February 2009): G266—G274. http://dx.doi.org/10.1152/ajpgi.90583.2008.

Full text
Abstract:
Hepatic ischemia-reperfusion (I/R) injury is an important complication of liver surgery and transplantation. Mitochondrial function is central to this injury. To examine alterations in mitochondrial function during I/R, we assessed the mitochondrial proteome in C57Bl/6 mice. Proteomic analysis of liver mitochondria revealed 234 proteins with significantly altered expression after I/R. From these, 13 proteins with the greatest expression differences were identified. One of these proteins, peroxiredoxin-6 (Prdx6), has never before been described in mitochondria. In hepatocytes from sham-operated mice, Prdx6 expression was found exclusively in the cytoplasm. After ischemia or I/R, Prdx6 expression disappeared from the cytoplasm and appeared in the mitochondria, suggesting mitochondrial trafficking. To explore the functional role of Prdx6 in hepatic I/R injury, wild-type and Prdx6-knockout mice were subjected to I/R injury. Prdx6-knockout mice had significantly more hepatocellular injury compared with wild-type mice. Interestingly, the increased injury in Prdx6-knockout mice occurred despite reduced inflammation and was associated with increased mitochondrial generation of H2O2 and dysfunction. The mitochondrial dysfunction appeared to be related to complex I of the electron transport chain. These data suggest that hepatocyte Prdx6 traffics to the mitochondria during I/R to limit mitochondrial dysfunction as a protective mechanism against hepatocellular injury.
APA, Harvard, Vancouver, ISO, and other styles
6

Fokin, Andrej, Rasa Žūkienė, and Aivaras Ratkevičius. "REDUCED CITRATE SYNTHASE ACTIVITY EFFECT ON OXYGEN CONSUMPTION RATES IN ISOLATED MITOCHONDRIA FROM MICE LIVER AND MUSCLES." Baltic Journal of Sport and Health Sciences 2, no. 101 (2016): 26–30. http://dx.doi.org/10.33607/bjshs.v2i101.52.

Full text
Abstract:
Background. Liver and skeletal muscles play the major role in metabolism. Mitochondria are of particular importance in functioning of these organs. We tested the hypothesis that reduced citrate synthase (CS) activity could induce improved fatty substrate and carbohydrate oxidation in mitochondria extracted from liver and hind limb muscles of mice. Methods. Eight mice each of 12-week-old control C57B6/J (B6) and congenic B6.A-(rs3676616-D10Utsw1)/ Kjn (B6.A) mice were studied. The mitochondria were isolated by differential centrifugation method followed by assessment of mitochondrial respiration and citrate synthase (CS) activity. Mitochondrial respiration was measured as oxygen consumption with Clark-type oxygen electrode by using polarography system. CS enzyme activity was measured spectrophotometrically. Results. The activity of CS was by ~32% lower for mitochondria for B6.A compared to B6 mice (603.9 ± 135.6 U/g and 894.2 ± 193.2 U/g, respectively). Mitochondrial respiration did not differ significantly between the strains. Conclusions. 30% reduction in citrate synthase activity does not impair mitochondrial respiration.
APA, Harvard, Vancouver, ISO, and other styles
7

SPEER, Oliver, Nils BÄCK, Tanja BUERKLEN, Dieter BRDICZKA, Alan KORETSKY, Theo WALLIMANN, and Ove ERIKSSON. "Octameric mitochondrial creatine kinase induces and stabilizes contact sites between the inner and outer membrane." Biochemical Journal 385, no. 2 (January 7, 2005): 445–50. http://dx.doi.org/10.1042/bj20040386.

Full text
Abstract:
We have investigated the role of the protein ubiquitous mitochondrial creatine kinase (uMtCK) in the formation and stabilization of inner and outer membrane contact sites. Using liver mitochondria isolated from transgenic mice, which, unlike control animals, express uMtCK in the liver, we found that the enzyme was associated with the mitochondrial membranes and, in addition, was located in membrane-coated matrix inclusions. In mitochondria isolated from uMtCK transgenic mice, the number of contact sites increased 3-fold compared with that observed in control mitochondria. Furthermore, uMtCK-containing mitochondria were more resistant to detergent-induced lysis than wild-type mitochondria. We conclude that octameric uMtCK induces the formation of mitochondrial contact sites, leading to membrane cross-linking and to an increased stability of the mitochondrial membrane architecture.
APA, Harvard, Vancouver, ISO, and other styles
8

Hamilton, James, Tatiana Brustovetsky, Rajesh Khanna, and Nickolay Brustovetsky. "Mutant huntingtin does not cross the mitochondrial outer membrane." Human Molecular Genetics 29, no. 17 (August 21, 2020): 2962–75. http://dx.doi.org/10.1093/hmg/ddaa185.

Full text
Abstract:
Abstract Mutant huntingtin (mHTT) is associated with mitochondria, but the exact mitochondrial location of mHTT has not been definitively established. Recently, it was reported that mHTT is present in the intermembrane space and inhibits mitochondrial protein import by interacting with TIM23, a major component of mitochondrial protein import machinery, but evidence for functional ramifications were not provided. We assessed mHTT location using synaptic and nonsynaptic mitochondria isolated from brains of YAC128 mice and subjected to alkali treatment or limited trypsin digestion. Mitochondria were purified either with discontinuous Percoll gradient or with anti-TOM22-conjugated iron microbeads. We also used mitochondria isolated from postmortem brain tissues of unaffected individuals and HD patients. Our results demonstrate that mHTT is located on the cytosolic side of the mitochondrial outer membrane (MOM) but does not cross it. This refutes the hypothesis that mHTT may interact with TIM23 and inhibit mitochondrial protein import. The levels of expression of nuclear-encoded, TIM23-transported mitochondrial proteins ACO2, TUFM, IDH3A, CLPP and mitochondrially encoded and synthesized protein mtCO1 were similar in mitochondria from YAC128 mice and their wild-type littermates as well as in mitochondria from postmortem brain tissues of unaffected individuals and HD patients, supporting the lack of deficit in mitochondrial protein import. Regardless of purification technique, mitochondria from YAC128 and WT mice had similar respiratory activities and mitochondrial membrane potentials. Thus, our data argue against mHTT crossing the MOM and entering into the mitochondrial intermembrane space, making it highly unlikely that mHTT interacts with TIM23 and inhibits protein import in intact mitochondria.
APA, Harvard, Vancouver, ISO, and other styles
9

Martin, George M., and Lawrence A. Loeb. "Mice and mitochondria." Nature 429, no. 6990 (May 2004): 357–59. http://dx.doi.org/10.1038/429357a.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Kuznetsov, Andrey V., Oleg Mayboroda, Dagmar Kunz, Kirstin Winkler, Walter Schubert, and Wolfram S. Kunz. "Functional Imaging of Mitochondria in Saponin-permeabilized Mice Muscle Fibers." Journal of Cell Biology 140, no. 5 (March 9, 1998): 1091–99. http://dx.doi.org/10.1083/jcb.140.5.1091.

Full text
Abstract:
Confocal laser-scanning and digital fluorescence imaging microscopy were used to quantify the mitochondrial autofluorescence changes of NAD(P)H and flavoproteins in unfixed saponin-permeabilized myofibers from mice quadriceps muscle tissue. Addition of mitochondrial substrates, ADP, or cyanide led to redox state changes of the mitochondrial NAD system. These changes were detected by ratio imaging of the autofluorescence intensities of fluorescent flavoproteins and NAD(P)H, showing inverse fluorescence behavior. The flavoprotein signal was colocalized with the potentiometric mitochondria-specific dye dimethylaminostyryl pyridyl methyl iodide (DASPMI), or with MitoTracker™ Green FM, a constitutive marker for mitochondria. Within individual myofibers we detected topological mitochondrial subsets with distinct flavoprotein autofluorescence levels, equally responding to induced rate changes of the oxidative phosphorylation. The flavoprotein autofluorescence levels of these subsets differed by a factor of four. This heterogeneity was substantiated by flow-cytometric analysis of flavoprotein and DASPMI fluorescence changes of individual mitochondria isolated from mice skeletal muscle. Our data provide direct evidence that mitochondria in single myofibers are distinct subsets at the level of an intrinsic fluorescent marker of the mitochondrial NAD–redox system. Under the present experimental conditions these subsets show similar functional responses.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Mice Mitochondria"

1

Vermulst, Marc. "Untangling mitochondrial mutagenesis and aging in mice /." Thesis, Connect to this title online; UW restricted, 2008. http://hdl.handle.net/1773/6321.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Kawashima, Tsuneaki. "Constitutive SIRT1 overexpression impairs mitochondria and reduces cardiac function in mice." Kyoto University, 2012. http://hdl.handle.net/2433/157426.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Jugé, Romain. "Étude de la dynamique mitochondriale dans des cellules cutanées humaines : Mise en place de modèles pour des applications en cosmétologie." Thesis, Lyon, 2016. http://www.theses.fr/2016LYSEN007.

Full text
Abstract:
La peau est un épithélium spécialisé vital et fragile, qui évolue avec l’âge et est influencé par l’environnement, notamment les radiations solaires. Des données sont disponibles sur la réponse du réseau mitochondrial et le devenir des mitochondries endommagées en réponse à des stress chimiques et environnementaux dans plusieurs systèmes expérimentaux, mais ces processus restent peu étudiés dans les cellules cutanées. Dans ce contexte, le projet de thèse visait à analyser l’effet (i) de l’irradiation UVB sur la dynamique mitochondriale (en particulier la fragmentation des mitochondries) dans des kératinocytes primaires humains normaux, qui constituent la première ligne de défense contre les agressions externes ; (ii) d’un traitement par des poisons mitochondriaux sur les mitochondries contenues dans des kératinocytes ou des fibroblastes primaires humains normaux. Dans un premier axe de la thèse, nous avons mis au point une méthode originale (Mitoshape) basée sur l’imagerie confocale, permettant d’estimer à la fois qualitativement et quantitativement la morphologie du réseau mitochondrial dans des cellules vivantes après irradiation UVB. Grâce à cette technologie, nous avons pu montrer que les UVB induisaient une fragmentation du réseau mitochondrial dans les kératinocytes primaires, dont nous avons étudié les acteurs biochimiques. Dans un deuxième axe, nous avons montré que les poisons mitochondriaux avaient la capacité d’endommager les mitochondries dans des kératinocytes et des fibroblastes humains primaires et induisaient une autophagie générale sans toutefois exclure la présence d’une mitophagie dépendante de la voie PINK1/PARKIN. Outre son intérêt fondamental, ce travail (réalisé en collaboration avec la société de cosmétologie SILAB dans le cadre d’un partenariat industriel CIFRE) ouvre la voie à l’identification d’actifs naturels capables de préserver et/ou restaurer les paramètres fonctionnels mitochondriaux suite à des stress
The skin is a specialized type of epithelium, both vital and fragile, which evolves with age and is continuously exposed to environmental stresses, such as solar radiations. While data is available about the response of the mitochondrial network and the fate of damaged mitochondria after chemical or environmental stresses in numerous experimental systems, little is known about these processes in skin cells. The aim of the present thesis was to study the impact (i) of UVB irradiation on mitochondrial dynamics (especially mitochondrial fragmentation) in normal human epidermal keratinocytes, which represent the first line of defence against environmental insults; (ii) of poisoning mitochondria of keratinocytes and normal human fibroblasts with chemical drugs. In a first axis, we developed an original method (called Mitoshape) based on confocal microscopy, to estimate qualitatively and quantitatively the morphology of the mitochondrial network within live cells following UVB irradiation. Using this technology, we demonstrated that UVB irradiation induces mitochondrial fragmentation in normal human keratinocytes, and studied the biochemical actors involved in this response. In a second axis, we showed that the use of mitochondrial poisons could damage mitochondria of keratinocytes and normal human fibroblasts and induce bulk autophagy, although it is not possible to formally rule out the involvement of a PINK1/PARKIN-dependent pathway of mitophagy. In addition to its fundamental interest, this work (performed in collaboration with the cosmetic company SILAB in the context of a CIFRE PhD fellowship from ANRT) paves the way for the screening of novel bioactive agents able to protect and restore mitochondria following stresses
APA, Harvard, Vancouver, ISO, and other styles
4

Puddick, Jonathan. "A comparative proteomics approach to studying skeletal muscle mitochondria from myostatin knockout mice." The University of Waikato, 2006. http://hdl.handle.net/10289/2254.

Full text
Abstract:
Myostatin is a negative regulator of muscle growth. When it is not present or non-functional double-muscling occurs, the primary characteristic of this phenotype being an increase in muscle mass. Another characteristic of double-muscling is an increased proportion of type IIB muscle fibres, which rely on glycolysis as their primary energy source, as opposed to type IIA and type I fibres which rely on oxidative phosphorylation. This switch in muscle metabolism directly impacts on the mitochondria, as mitochondria from glycolytic muscle fibres have been shown to have differences in metabolic activity. The increased proportion of glycolytic muscle fibres present in myostatin knockout animals provides a unique model to investigate alterations in muscle fibre type metabolism. The mouse model of myostatin knockout utilised during this study was generated by genetic deletion of exon three of the myostatin gene. Verification of this knockout was attempted by western blot analysis, but only the latency associated protein (LAP) was detected. Interestingly, the LAP was barely detectable in the knockout muscle suggesting deletion of exon three affects binding of anti-myostatin antibodies to the LAP, as that part of the gene is not deleted. A comparison of the basal mitochondrial stress levels was made, also by western blot analysis. The knockout mitochondria showed no change in levels of heat shock protein 60 or superoxide dismutase 2, indicating that they are not being subjected to any increased stress due to the myostatin knockout phenotype. A comparative proteomics approach was used to detect changes in the mitochondrial proteome of myostatin knockout gastrocnemius muscle to gain clues to how mitochondria from glycolytic muscle fibres differ from those present in oxidative fibres. This was undertaken using two-dimensional electrophoresis (2-DE), in-gel tryptic digests and peptide mass fingerprinting by mass spectrometry. A 2-DE gel protein loading of 220 g was shown to give the best protein spot resolution and the most crucial step in the loading process was found to be the laying of the immobilized pH gradient, which had to be performed very carefully to obtain a consistent loading pattern. This study resolved only around 160 protein spots out of the estimated 1,000 to 2,000 proteins present in the mitochondria. Modulation of six proteins was seen at a plt0.1 level, but were unable to be identified using the current methodology. More abundant mitochondrial proteins were able to be identified, but showed no significant modulation. Malate dehydrogenase and 3-hydroxyacyl-CoA dehydrogenase, which were identified during this study, have been reported to have decreased activity in mitochondria from glycolytic muscle fibres. This study suggests that the change in activity observed by other researchers is due to inhibition of these enzymes in the glycolytic fibres or activation in the oxidative fibres.
APA, Harvard, Vancouver, ISO, and other styles
5

Pan, Minglin, Ying Han, Rui Si, Rui Guo, Ankit Desai, and Ayako Makino. "Hypoxia-induced pulmonary hypertension in type 2 diabetic mice." SAGE PUBLICATIONS INC, 2017. http://hdl.handle.net/10150/623894.

Full text
Abstract:
Hypoxia-induced pulmonary hypertension (HPH) is a progressive disease that is mainly caused by chronic exposure to high altitude, chronic obstructive lung disease, and obstructive sleep apnea. The increased pulmonary vascular resistance and increased pulmonary arterial pressure result in increased right ventricular afterload, leading to right heart failure and increased morbidity. There are several clinical reports suggesting a link between PH and diabetes, insulin resistance, or obesity; however, it is unclear whether HPH is associated with diabetes as a progressive complication in diabetes. The major goal of this study is to examine the effect of diabetic ''preconditioning'' or priming effect on the progression of HPH and define the molecular mechanisms that explain the link between diabetes and HPH. Our data show that HPH is significantly enhanced in diabetic mice, while endothelium-dependent relaxation in pulmonary arteries is significantly attenuated in chronically hypoxic diabetic mice (DH). In addition, we demonstrate that mouse pulmonary endothelial cells (MPECs) isolated from DH mice exhibit a significant increase in mitochondrial reactive oxygen species (ROS) concentration and decreased SOD2 protein expression. Finally, scavenging mitochondrial ROS by mitoTempol restores endothelium-dependent relaxation in pulmonary arteries that is attenuated in DH mice. These data suggest that excessive mitochondrial ROS production in diabetic MPECs leads to the development of severe HPH in diabetic mice exposed to hypoxia.
APA, Harvard, Vancouver, ISO, and other styles
6

Barros, Susana Raquel Costa. "Metabolic adaptations in liver-specific OPA1 knockout mice." Doctoral thesis, Universitat de Barcelona, 2020. http://hdl.handle.net/10803/668803.

Full text
Abstract:
OPA1 is a dynamin-related protein that is responsible for the fusion of the internal mitochondrial membrane and essential to control the morphology of the mitochondrial cristae. Thus, it directly impacts the efficiency of OxPhos and the stability of mitochondrial DNA. In this study, we have explored the effects of hepatic deletion of OPA1 on mitochondrial function and metabolism. We have shown that the ablation of OPA1 in the liver produces a mitochondrial dysfunction characterized by alterations in mitochondrial cristae structure, concomitant with a reduced respiratory capacity and mtDNA copy number, and perturbed mitochondrial proteostasis. The mitochondrial dysfunction caused by the ablation of OPA1 in liver triggers the activation of a mitochondrial stress response, including mitochondrial unfolded stress response (UPRmt) that is probably mediated by the transcription factor ATF5. Interestingly, we have observed that OPA1 deficiency in the liver causes better glucose tolerance and protects against diet-induced obesity and insulin resistance concomitant to a high circulating levels of the metabolic modulator FGF21. Here we suggest that the systemic protective effects associated to OPA1 ablation are due to the action of FGF21, probably mediated by the mitochondrial stress response associated to OPA1 loss- of-function via ATF5 activation.
OPA1 es una proteína relacionada con la dinamina que es responsable de la fusión de la membrana mitocondrial interna y esencial para controlar la morfología de las crestas mitocondriales, afectando directamente la eficiencia de OxPhos y la estabilidad del DNA mitocondrial. En este estudio, hemos explorado los efectos de la eliminación hepática de OPA1 sobre la función mitocondrial y el metabolismo. Hemos demostrado que la ablación de OPA1 en el hígado produce una disfunción mitocondrial caracterizada por alteraciones en la estructura de las crestas mitocondriales, concomitante con una capacidad respiratoria reducida y menor número de copias de DNA miocondrial, y perturbación en la proteostasis mitocondrial. La disfunción mitocondrial causada por la ablación de OPA1 en el hígado desencadena la activación de una respuesta al estrés mitocondrial, incluyendo la respuesta a las proteínas mal plegadas de la mitocondria, que probablemente es mediada por el factor de transcripción ATF5. Curiosamente, hemos observado que la deficiencia de OPA1 en el hígado causa una mejor tolerancia a la glucosa y protege contra la obesidad y resistencia a la insulina inducida por la dieta, en paralelo con un aumento de los niveles de FGF21 circulante, un factor involucrado en la modulación metabólica. Con este estudio proponemos que los efectos sistémicos protectores asociados a la ablación de OPA1 se deben a la acción de FGF21 que probablemente es mediada por la respuesta al estrés mitocondrial asociada a la pérdida de función de OPA1 a través de la activación de ATF5.
APA, Harvard, Vancouver, ISO, and other styles
7

Beauchamp, Brittany. "Low Birth Weight is Associated with Impaired Skeletal and Cardiac Muscle Energetics in Adult Mice." Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/32963.

Full text
Abstract:
In utero undernutrition is associated with increased risk for insulin resistance, obesity, and cardiovascular disease during adult life. A common phenotype associated with low birth weight is reduced skeletal muscle mass. Given the central role of skeletal muscle in whole body metabolism, we hypothesized that predisposition to metabolic disease is, in part, due to low oxidative capacity and dysfunctional mitochondrial energetics in muscle. We used an experimental mouse model system of maternal undernutrition during late pregnancy to examine female offspring from undernourished dams (U) and control offspring from ad libitum fed dams (C). U have increased adiposity and decreased glucose tolerance compared to C. Strikingly, when U are put on a 4 week 40% calorie restricted diet they lose half as much weight as calorie restricted controls. Skeletal muscle mitochondria from U have decreased coupled and uncoupled respiration and increased maximal respiration compared to C. In permeabilized fiber preparations from mixed fiber type muscle, U have decreased mitochondrial content and decreased adenylate free leak respiration, fatty acid oxidative capacity, and state 3 respiratory capacity through complex I. Fiber maximal oxidative phosphorylation capacity does not differ between U and C. We next aimed to determine if the impaired skeletal muscle energetics observed in U also exist in primary muscle cells derived from these mice. We measured oxidative and glycolytic capacities in primary myotubes from U and C using cellular bioenergetics. Myotubes from U have decreased resting respiration and increased glycolysis compared to myotubes from C. There was no difference in myotube mitochondrial content. Findings suggest that undernutrition in utero causes a primary muscle defect. Energetics in cardiac muscle were also examined. U have impaired cardiac muscle homogenate energetics, including decreased fatty acid oxidative capacity, decreased maximum oxidative phosphorylation rate, and decreased proton leak respiration. Additionally, we measured plasma acylcarnitine levels and found that short-chain acylcarnitines are increased in U. Overall, results reveal that in utero undernutrition alters metabolic physiology through a profound effect on skeletal muscle and cardiac muscle energetics. These effects may be mediated by epigenetic mechanisms which could be explored in future research.
APA, Harvard, Vancouver, ISO, and other styles
8

Alshudukhi, Abdullah Ali. "Exploring the role of lipin1 in mitophagy process using lipin1 deficient-EGFP tagged LC3 transgenic mice." Wright State University / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=wright151377463726015.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Luther, Daniel J. "The Role of Type VI Collagen In Cardiac Remodeling Following Myocardial Infarction In Mice." Kent State University / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=kent1376067347.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Chen, Z. (Zhijun). "Characterization of the 2-enoyl thioester reductase of mitochondrial fatty acid synthesis type II in mammals." Doctoral thesis, University of Oulu, 2008. http://urn.fi/urn:isbn:9789514289804.

Full text
Abstract:
Abstract A data base search using the amino acid sequence of Saccharomyces cerevisiae Etr1p, the last enzyme of mitochondrial fatty acid synthesis type II (FAS II), revealed a highly similar human protein, NRBF-1. Expression of NRBF-1 in a yeast etr1Δ strain rescued its respiratory deficiency. NRBF-1 resides in mitochondria in cultured HeLa cells. The recombinant NRBF-1 is enzymatically active, reducing 2E-enoyl-CoAs to acyl-CoAs in an NADPH-dependent manner. Altogether, our data showed that NRBF-1 is a mitochondrial 2-enoyl-CoA reductase/2-enoyl thioester reductase (MECR/ETR1), the human functional counterpart of yeast Etr1p. In addition, MECR was also isolated from bovine heart. It turns out that mammals contain a mitochondrial FAS II pathway, in addition to cytoplasmic FAS I. To investigate the functional mechanism of MECR/ETR1 at the molecular level, the protein was crystallized and the crystal structure determined. The apo-structure of MECR/ETR1 contains two sulfates in the nucleotide binding site and the domain arrangement resembles the NADPH-containing holo-structure of yeast Etr1p. The predicted mode of NADPH-binding and kinetic data suggest that Tyr94 and Trp311 play critical roles in catalysis. A pocket was found in the structure extending away from the catalytic site that can accommodate fatty acyl chains up to 16 carbons. An acyl carrier protein (ACP) binding site was also suggested. To study the physiological function of mouse Mecr, two lines of transgenic mice overexpressing Mecr were generated. The Mecr transgenic mice developed cardiac and mitochondrial abnormalities. The phenotyping was carried out using echocardiography, heart perfusion, histology, and endurance testing. Our results suggest Mecr plays a role in mitochondrial and heart function. Therefore, inappropriate expression of the genes of FAS II may result in the development of cardiomyopathy.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Mice Mitochondria"

1

Wortley, Janette. The putative association of peroxisomes and mitochondria in lean and obese mice. Wolverhampton: University of Wolverhampton, 1996.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Will, Yvonne. Use of Þ-Glutamyltranspeptidase-deficient knockout mice as a model to study the relationship between glutathione status, mitochondrial dysfunction, and cell death. 1999.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Will, Yvonne. Use of Þ-Glutamyltranspeptidase-deficient knockout mice as a model to study the relationship between glutathione status, mitochondrial dysfunction, and cell death. 1999.

Find full text
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "Mice Mitochondria"

1

Singh, P. J., J. Legault, A. Tremblay, P. Julien, M. R. Ven Murthy, and M. E. Mirault. "PCR analysis of mitochondrial DNA from normal and transgenic glutathione peroxidase mice." In Oxidative Stress and Aging, 179–90. Basel: Birkhäuser Basel, 1995. http://dx.doi.org/10.1007/978-3-0348-7337-6_19.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Kolbe, Thomas, Ralf Steinborn, and Joerg P. Burgstaller. "Cytoplasmic Transfer Methods for Studying the Segregation of Mitochondrial DNA in Mice." In Methods in Molecular Biology, 357–65. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2288-8_25.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Kolbe, Thomas, Ralf Steinborn, and Joerg P. Burgstaller. "Cytoplasmic Transfer Methods for Studying the Segregation of Mitochondrial DNA in Mice." In Methods in Molecular Biology, 91–99. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1270-5_6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Anflous, Keltoum, and William J. Craigen. "Mitochondrial Porins in Mammals: Insights into Functional Roles from Mutant Mice and Cells." In Bacterial and Eukaryotic Porins, 285–307. Weinheim, FRG: Wiley-VCH Verlag GmbH & Co. KGaA, 2005. http://dx.doi.org/10.1002/3527603875.ch14.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Gomez-Niño, Angela, Inmaculada Docio, Jesus Prieto-Lloret, Maria Simarro, Miguel A. de la Fuente, and Asuncion Rocher. "Mitochondrial Complex I Dysfunction and Peripheral Chemoreflex Sensitivity in a FASTK-Deficient Mice Model." In Advances in Experimental Medicine and Biology, 51–59. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-91137-3_6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Wang, Qilong, and Ming-Hui Zou. "Measurement of Reactive Oxygen Species (ROS) and Mitochondrial ROS in AMPK Knockout Mice Blood Vessels." In Methods in Molecular Biology, 507–17. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7598-3_32.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Takahashi, Yoshinori, Koichiro Kako, Hidenori Arai, Akio Takehara, and Eisuke Munekata. "Effect of Deficiency of Cytochrome C Oxidase Assembly Peptide Cox17p on Mitochondrial Functions and Respiratory-Chain in Mice." In Peptides: The Wave of the Future, 795–96. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-010-0464-0_372.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Sawashita, Jinko, Xu Zhe, and Keiichi Higuchi. "Reduced Coenzyme Q10 Decelerates Senescence and Age-Related Hearing Loss in Senescence-Accelerated Mice by Activating Mitochondrial Functions." In Coenzyme Q in Aging, 169–87. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-45642-9_9.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Laouafa, Sofien, Damien Roussel, François Marcouiller, Jorge Soliz, Aida Bairam, and Vincent Joseph. "Role of Estradiol Receptor Beta (ERβ) on Arterial Pressure, Respiratory Chemoreflex and Mitochondrial Function in Young and Aged Female Mice." In Advances in Experimental Medicine and Biology, 115–27. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-91137-3_15.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Nishiyama, Takahisa, Erika Hasegawa, Shigeru Yanagi, Yoshihisa Kudo, Ryuta Hamada, Noriko Matsumura, Mikiko Tomino, Yukio Muromachi, Kiyoshi Hatakeyama, and Hiroyuki Uchino. "Simultaneous Measurement of Cytosolic and Mitochondrial Ca2+ During Ischemia in Mice Whole-Brain Slice Preparation and Its Application to Drug Evaluation." In Brain Edema XV, 65–70. Vienna: Springer Vienna, 2013. http://dx.doi.org/10.1007/978-3-7091-1434-6_11.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Mice Mitochondria"

1

Kumar, V., A. Brown, L. Balachandran, J. Horvat, M. Whiteman, and P. Hansbro. "Targeting Mitochondria with Hydrogen Sulphide Attenuates Cigarettes Smoke-Induced Mitochondrial Dysfunction, Oxidative Damage, Inflammation and Lung Injury in Mice." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a1241.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Matveyenko, Olga A., Maxim E. Komnatnov, Anna V. Busygina, and Lubov P. Zharkova. "Study of impact of picosecond pulses on functional status of mitochondria of mice liver in TEM-cell." In 2016 17th International Conference of Young Specialists on Micro/Nanotechnologies and Electron Devices (EDM). IEEE, 2016. http://dx.doi.org/10.1109/edm.2016.7538818.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Ufimtseva, Elena. "MITOCHONDRIA AND ANTIAPOPTOTIC PROTEIN BCL-2 IN MYCOBACTERIUM-HOST CELL RELATIONSHIPS IN GRANULOMAS OF MICE WITH LATENT TUBERCULOUS INFECTION." 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/10.31255/978-5-94797-318-1-139-141.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Karaman-Kutluay, Yasemin, Yesim Kaya-Yasar, Turgut Emrah Bozkurt, Sevgen Celik Onder, and Inci Sahin-Erdemli. "Intranasal treatment with the mitochondria-targeted slow hydrogen sulfide releasing donor AP39 prevents inflammation-induced airway hyperreactivity in mice." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa3879.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Heyob, KM, LK Rogers, and SE Welty. "Transgenic Mice with Glutathione Reductase Targeted to the Mitochondria of Type II Cells Are Not Riboflavin Deficient in Hyperoxia." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5004.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Losier, A. J., L. K. Sharma, Y. Zhang, W. Liu, P. Lee, and C. Dela Cruz. "Streptococcus Pneumoniae Pneumonia Induces Mitochondrial Biogenesis and Antioxidant Responses in Mice." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a5595.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Maskell, Lauren, Daniel Stuckey, and Vishwanie Budhram-Mahadeo. "P36 Loss of POU4F2/BRN3B in the stressed heart compromises the adaptive hypertrophic response in male BRN3B ko mice, but not BRN3B ko female mice." In British Society for Cardiovascular Research, Autumn Meeting 2017 ‘Cardiac Metabolic Disorders and Mitochondrial Dysfunction’, 11–12 September 2017, University of Oxford. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2018-bscr.41.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Springer, C., C. Binsch, L. Toska, M. Lienhard, R. Herwig, A. Chadt, and H. Al-Hasani. "Altered skeletal muscle mitochondrial gene expression contributes to exercise non-response in hyperglycaemic NZO mice." In Diabetes Kongress 2019 – 54. Jahrestagung der DDG. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1688157.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Pouwels, Simon, Nick Ten Hacken, Jaap Lubbers, Antoon Van Oosterhout, Martijn Nawijn, and Irene Heijink. "The human cathelicidin LL37 and mitochondrial DAMPs induce airway inflammation in epithelial cells and mice." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa5115.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Bléhaut, Tanguy RW, Matthew TG Gibbins, Simon Horvat, Patrick WF Hadoke, and Nicholas M. Morton. "O2 Deficiency of the mitochondrial hydrogen sulfide clearance enzyme thiosulfate sulfurtransferase ameliorates atherosclerosis in Apoe-knockout mice." In The Scottish Cardiovascular Forum 2019, Saturday 2nd February 2019, The Centre for Health Science, Old Perth Road, Inverness, Scotland. BMJ Publishing Group Ltd and British Cardiovascular Society, 2019. http://dx.doi.org/10.1136/heartjnl-2019-scf.5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Mice Mitochondria' for particular source types:
Journal articles Dissertations / Theses
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography