Journal articles on the topic 'Transmission mitochondriale'
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1
Wilhelm, J. M., B. Mousson de Camaret, A. Derragui, R. Dukic, P. Thannberger, O. Saraceni, and P. Kieffer. "Ophtalmoplégie progressive chronique ≪ plus ≫d'origine mitochondriale à transmission autosomique dominante." La Revue de Médecine Interne 24 (December 2003): 465s. http://dx.doi.org/10.1016/s0248-8663(03)80555-6.
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Angers, Annie, Philip Ouimet, Assia Tsyvian-Dzyabko, Tanya Nock, and Sophie Breton. "L’ADN mitochondrial, un potentiel codant mésestimé." médecine/sciences 35, no. 1 (January 2019): 46–54. http://dx.doi.org/10.1051/medsci/2018308.
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Du génome bactérien de l’endosymbionte d’origine les mitochondries animales n’ont retenu que 13 séquences codant des polypeptides essentiels à la production d’ATP. La découverte de petits peptides d’origine mitochondriale vient remettre en question cette interprétation du génome des mitochondries et suggère que leur potentiel codant reste sous-estimé. L’humanine, MOTS-c, les SHLP et Gau sont des peptides dérivés de l’ADN mitochondrial dont l’existence a été démontrée expérimentalement et qui jouent des rôles importants dans la régulation de l’apoptose et du métabolisme cellulaire. Chez certains bivalves à transmission doublement uniparentale des mitochondries, des gènes codant des peptides additionnels ont été découverts et pourraient être impliqués dans la détermination du sexe de ces animaux.
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Pierry, C., T. Trian, E. Maurat, R. Marthan, P. O. Girodet, and P. Berger. "Ultrastructure mitochondriale du muscle lisse bronchique chez l’asthmatique sévère et non sévère : étude quantitative en microscopie électronique à transmission." Revue des Maladies Respiratoires 34 (January 2017): A328—A329. http://dx.doi.org/10.1016/j.rmr.2016.10.868.
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Pierry, C., T. Trian, E. Maurat, R. Marthan, P. O. Girodet, and P. Berger. "Ultrastructure mitochondriale du muscle lisse bronchique chez l’asthmatique sévère et non sévère : étude quantitative en miscroscopie électronique à transmission." Revue des Maladies Respiratoires 34 (January 2017): A26—A27. http://dx.doi.org/10.1016/j.rmr.2016.10.056.
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Wilhelm, J. M., B. Mousson de Camret, S. Rozan-Rodier, A. Derragui, P. Thannberger, and O. Saraceni. "P120 Diabète associé à une cytopathie mitochondriale à transmission autosomique dominante. À propos d’un cas de mutation du gène nucléaire Twinkle." Diabetes & Metabolism 35 (March 2009): A56. http://dx.doi.org/10.1016/s1262-3636(09)71918-4.
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Yancey, Danielle M., Jason L. Guichard, Mustafa I. Ahmed, Lufang Zhou, Michael P. Murphy, Michelle S. Johnson, Gloria A. Benavides, James Collawn, Victor Darley-Usmar, and Louis J. Dell'Italia. "Cardiomyocyte mitochondrial oxidative stress and cytoskeletal breakdown in the heart with a primary volume overload." American Journal of Physiology-Heart and Circulatory Physiology 308, no. 6 (March 15, 2015): H651—H663. http://dx.doi.org/10.1152/ajpheart.00638.2014.
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Left ventricular (LV) volume overload (VO) results in cardiomyocyte oxidative stress and mitochondrial dysfunction. Because mitochondria are both a source and target of ROS, we hypothesized that the mitochondrially targeted antioxidant mitoubiquinone (MitoQ) will improve cardiomyocyte damage and LV dysfunction in VO. Isolated cardiomyocytes from Sprague-Dawley rats were exposed to stretch in vitro and VO of aortocaval fistula (ACF) in vivo. ACF rats were treated with and without MitoQ. Isolated cardiomyocytes were analyzed after 3 h of cyclical stretch or 8 wk of ACF with MitoSox red or 5-(and-6)-chloromethyl-2′,7′-dichlorodihydrofluorescein diacetate to measure ROS and with tetramethylrhodamine to measure mitochondrial membrane potential. Transmission electron microscopy and immunohistochemistry were used for cardiomyocyte structural assessment. In vitro cyclical stretch and 8-wk ACF resulted in increased cardiomyocyte mitochondrial ROS production and decreased mitochondrial membrane potential, which were significantly improved by MitoQ. ACF had extensive loss of desmin and β2-tubulin that was paralleled by mitochondrial disorganization, loss of cristae, swelling, and clustering identified by mitochondria complex IV staining and transmission electron microscopy. MitoQ improved mitochondrial structural damage and attenuated desmin loss/degradation evidenced by immunohistochemistry and protein expression. However, LV dilatation and fractional shortening were unaffected by MitoQ treatment in 8-wk ACF. In conclusion, although MitoQ did not affect LV dilatation or function in ACF, these experiments suggest a connection of cardiomyocyte mitochondria-derived ROS production with cytoskeletal disruption and mitochondrial damage in the VO of ACF.
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Medler, Kathryn, and Evanna L. Gleason. "Mitochondrial Ca2+ Buffering Regulates Synaptic Transmission Between Retinal Amacrine Cells." Journal of Neurophysiology 87, no. 3 (March 1, 2002): 1426–39. http://dx.doi.org/10.1152/jn.00627.2001.
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The diverse functions of retinal amacrine cells are reliant on the physiological properties of their synapses. Here we examine the role of mitochondria as Ca2+ buffering organelles in synaptic transmission between GABAergic amacrine cells. We used the protonophore p-trifluoromethoxy-phenylhydrazone (FCCP) to dissipate the membrane potential across the inner mitochondrial membrane that normally sustains the activity of the mitochondrial Ca2+ uniporter. Measurements of cytosolic Ca2+ levels reveal that prolonged depolarization-induced Ca2+ elevations measured at the cell body are altered by inhibition of mitochondrial Ca2+ uptake. Furthermore, an analysis of the ratio of Ca2+ efflux on the plasma membrane Na-Ca exchanger to influx through Ca2+ channels during voltage steps indicates that mitochondria can also buffer Ca2+ loads induced by relatively brief stimuli. Importantly, we also demonstrate that mitochondrial Ca2+ uptake operates at rest to help maintain low cytosolic Ca2+ levels. This aspect of mitochondrial Ca2+ buffering suggests that in amacrine cells, the normal function of Ca2+-dependent mechanisms would be contingent upon ongoing mitochondrial Ca2+ uptake. To test the role of mitochondrial Ca2+ buffering at amacrine cell synapses, we record from amacrine cells receiving GABAergic synaptic input. The Ca2+ elevations produced by inhibition of mitochondrial Ca2+uptake are localized and sufficient in magnitude to stimulate exocytosis, indicating that mitochondria help to maintain low levels of exocytosis at rest. However, we found that inhibition of mitochondrial Ca2+ uptake during evoked synaptic transmission results in a reduction in the charge transferred at the synapse. Recordings from isolated amacrine cells reveal that this is most likely due to the increase in the inactivation of presynaptic Ca2+ channels observed in the absence of mitochondrial Ca2+ buffering. These results demonstrate that mitochondrial Ca2+ buffering plays a critical role in the function of amacrine cell synapses.
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Kitazaki, Kazuyoshi, and Tomohiko Kubo. "Cost of Having the Largest Mitochondrial Genome: Evolutionary Mechanism of Plant Mitochondrial Genome." Journal of Botany 2010 (May 30, 2010): 1–12. http://dx.doi.org/10.1155/2010/620137.
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The angiosperm mitochondrial genome is the largest and least gene-dense among the eukaryotes, because its intergenic regions are expanded. There seems to be no functional constraint on the size of the intergenic regions; angiosperms maintain the large mitochondrial genome size by a currently unknown mechanism. After a brief description of the angiosperm mitochondrial genome, this review focuses on our current knowledge of the mechanisms that control the maintenance and alteration of the genome. In both processes, the control of homologous recombination is crucial in terms of site and frequency. The copy numbers of various types of mitochondrial DNA molecules may also be controlled, especially during transmission of the mitochondrial genome from one generation to the next. An important characteristic of angiosperm mitochondria is that they contain polypeptides that are translated from open reading frames created as byproducts of genome alteration and that are generally nonfunctional. Such polypeptides have potential to evolve into functional ones responsible for mitochondrially encoded traits such as cytoplasmic male sterility or may be remnants of the former functional polypeptides.
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Aretz, Ina, Christopher Jakubke, and Christof Osman. "Power to the daughters – mitochondrial and mtDNA transmission during cell division." Biological Chemistry 401, no. 5 (April 28, 2020): 533–46. http://dx.doi.org/10.1515/hsz-2019-0337.
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AbstractMitochondria supply virtually all eukaryotic cells with energy through ATP production by oxidative phosphoryplation (OXPHOS). Accordingly, maintenance of mitochondrial function is fundamentally important to sustain cellular health and various diseases have been linked to mitochondrial dysfunction. Biogenesis of OXPHOS complexes crucially depends on mitochondrial DNA (mtDNA) that encodes essential subunits of the respiratory chain and is distributed in multiple copies throughout the mitochondrial network. During cell division, mitochondria, including mtDNA, need to be accurately apportioned to daughter cells. This process requires an intimate and coordinated interplay between the cell cycle, mitochondrial dynamics and the replication and distribution of mtDNA. Recent years have seen exciting advances in the elucidation of the mechanisms that facilitate these processes and essential key players have been identified. Moreover, segregation of qualitatively distinct mitochondria during asymmetric cell division is emerging as an important quality control step, which secures the maintenance of a healthy cell population.
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Su, Bo, Yun-Song Ji, Xu-lu Sun, Xiang-Hua Liu, and Zhe-Yu Chen. "Brain-derived Neurotrophic Factor (BDNF)-induced Mitochondrial Motility Arrest and Presynaptic Docking Contribute to BDNF-enhanced Synaptic Transmission." Journal of Biological Chemistry 289, no. 3 (December 3, 2013): 1213–26. http://dx.doi.org/10.1074/jbc.m113.526129.
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Appropriate mitochondrial transport and distribution are essential for neurons because of the high energy and Ca2+ buffering requirements at synapses. Brain-derived neurotrophic factor (BDNF) plays an essential role in regulating synaptic transmission and plasticity. However, whether and how BDNF can regulate mitochondrial transport and distribution are still unclear. Here, we find that in cultured hippocampal neurons, application of BDNF for 15 min decreased the percentage of moving mitochondria in axons, a process dependent on the activation of the TrkB receptor and its downstream PI3K and phospholipase-Cγ signaling pathways. Moreover, the BDNF-induced mitochondrial stopping requires the activation of transient receptor potential canonical 3 and 6 (TRPC3 and TRPC6) channels and elevated intracellular Ca2+ levels. The Ca2+ sensor Miro1 plays an important role in this process. Finally, the BDNF-induced mitochondrial stopping leads to the accumulation of more mitochondria at presynaptic sites. Mutant Miro1 lacking the ability to bind Ca2+ prevents BDNF-induced mitochondrial presynaptic accumulation and synaptic transmission, suggesting that Miro1-mediated mitochondrial motility is involved in BDNF-induced mitochondrial presynaptic docking and neurotransmission. Together, these data suggest that mitochondrial transport and distribution play essential roles in BDNF-mediated synaptic transmission.
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Zhang, Yi, and Hong Xu. "Translational regulation of mitochondrial biogenesis." Biochemical Society Transactions 44, no. 6 (December 2, 2016): 1717–24. http://dx.doi.org/10.1042/bst20160071c.
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Mitochondria are generated by the expression of genes on both nuclear and mitochondrial genome. Mitochondrial biogenesis is highly plastic in response to cellular energy demand, developmental signals and environmental stimuli. Mechanistic target of rapamycin (mTOR) pathway regulates mitochondrial biogenesis to co-ordinate energy homeostasis with cell growth. The local translation of mitochondrial proteins on the outer membrane facilitates their efficient import and thereby allows prodigious mitochondrial biogenesis during rapid cell growth and proliferation. We postulate that the local translation may also allow cells to promote mitochondrial biogenesis selectively based on the fitness of individual organelle. MDI–Larp complex promotes the biogenesis of healthy mitochondria and thereby is essential for the selective transmission of healthy mitochondria. On the other hand, PTEN-induced putative kinase 1 (PINK1)–Pakin activates protein synthesis on damaged mitochondria to maintain the organelle homeostasis and activity. We also summarize some recent progress on miRNAs' regulation on mitochondrial biogenesis.
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Nunnari, J., W. F. Marshall, A. Straight, A. Murray, J. W. Sedat, and P. Walter. "Mitochondrial transmission during mating in Saccharomyces cerevisiae is determined by mitochondrial fusion and fission and the intramitochondrial segregation of mitochondrial DNA." Molecular Biology of the Cell 8, no. 7 (July 1997): 1233–42. http://dx.doi.org/10.1091/mbc.8.7.1233.
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To gain insight into the process of mitochondrial transmission in yeast, we directly labeled mitochondrial proteins and mitochondrial DNA (mtDNA) and observed their fate after the fusion of two cells. To this end, mitochondrial proteins in haploid cells of opposite mating type were labeled with different fluorescent dyes and observed by fluorescence microscopy after mating of the cells. Parental mitochondrial protein markers rapidly redistributed and colocalized throughout zygotes, indicating that during mating, parental mitochondria fuse and their protein contents intermix, consistent with results previously obtained with a single parentally derived protein marker. Analysis of the three-dimensional structure and dynamics of mitochondria in living cells with wide-field fluorescence microscopy indicated that mitochondria form a single dynamic network, whose continuity is maintained by a balanced frequency of fission and fusion events. Thus, the complete mixing of mitochondrial proteins can be explained by the formation of one continuous mitochondrial compartment after mating. In marked contrast to the mixing of parental mitochondrial proteins after fusion, mtDNA (labeled with the thymidine analogue 5-bromodeoxyuridine) remained distinctly localized to one half of the zygotic cell. This observation provides a direct explanation for the genetically observed nonrandom patterns of mtDNA transmission. We propose that anchoring of mtDNA within the organelle is linked to an active segregation mechanism that ensures accurate inheritance of mtDNA along with the organelle.
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Milani, Liliana. "Mitochondrial membrane potential: a trait involved in organelle inheritance?" Biology Letters 11, no. 10 (October 2015): 20150732. http://dx.doi.org/10.1098/rsbl.2015.0732.
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Which mitochondria are inherited across generations? Are transmitted mitochondria functionally silenced to preserve the integrity of their genetic information, or rather are those mitochondria with the highest levels of function (as indicated by membrane potential Δ ψ m) preferentially transmitted? Based on observations of the unusual system of doubly uniparental inheritance of mitochondria and of the common strictly maternal inheritance mode, I formulate a general hypothesis to explain which mitochondria reach the primordial germ cells (PGCs), and how this happens. Several studies indicate that mitochondrial movements are driven by microtubules and that mitochondria with high Δ ψ m are preferentially transported. This can be applied also to the mitochondria that eventually populate embryonic PGCs, so I propose that Δ ψ m may be a trait that allows for the preferential transmission of the most active (and healthy) mitochondria. The topics discussed here are fundamental in cell biology and genetics but remain controversial and a subject of heated debate; I propose an explanation for how a Δ ψ m-dependent mechanism can cause the observed differences in mitochondrial transmission.
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Chidipi, Bojjibabu, Syed Islamuddin Shah, Michelle Reiser, Manasa Kanithi, Amanda Garces, Byeong J. Cha, Ghanim Ullah, and Sami F. Noujaim. "All-Trans Retinoic Acid Increases DRP1 Levels and Promotes Mitochondrial Fission." Cells 10, no. 5 (May 14, 2021): 1202. http://dx.doi.org/10.3390/cells10051202.
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In the heart, mitochondrial homeostasis is critical for sustaining normal function and optimal responses to metabolic and environmental stressors. Mitochondrial fusion and fission are thought to be necessary for maintaining a robust population of mitochondria, and disruptions in mitochondrial fission and/or fusion can lead to cellular dysfunction. The dynamin-related protein (DRP1) is an important mediator of mitochondrial fission. In this study, we investigated the direct effects of the micronutrient retinoid all-trans retinoic acid (ATRA) on the mitochondrial structure in vivo and in vitro using Western blot, confocal, and transmission electron microscopy, as well as mitochondrial network quantification using stochastic modeling. Our results showed that ATRA increases DRP1 protein levels, increases the localization of DRP1 to mitochondria in isolated mitochondrial preparations. Our results also suggested that ATRA remodels the mitochondrial ultrastructure where the mitochondrial area and perimeter were decreased and the circularity was increased. Microscopically, mitochondrial network remodeling is driven by an increased rate of fission over fusion events in ATRA, as suggested by our numerical modeling. In conclusion, ATRA results in a pharmacologically mediated increase in the DRP1 protein. It also results in the modulation of cardiac mitochondria by promoting fission events, altering the mitochondrial network, and modifying the ultrastructure of mitochondria in the heart.
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Hsiao, Yu-Han, Ching-Wen Li, Jui-Chih Chang, Sung-Tzu Chen, Chin-San Liu, and Gou-Jen Wang. "Chemical-Free Extraction of Functional Mitochondria Using a Microfluidic Device." Inventions 3, no. 4 (September 27, 2018): 68. http://dx.doi.org/10.3390/inventions3040068.
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This paper proposes the use of a chip-based microfluidic device to extract functional and chemical free mitochondria. A simple microfluidic device was designed and fabricated. An osteosarcoma cybrid cell line was employed to demonstrate the efficiency of the proposed microfluidic device. The membrane proteins (mitochondrial complex I-V and Tom20) and morphology of the extracted mitochondria were examined by Western blot and transmission electron microscopy (TEM), respectively. The purity and mitochondrial membrane potential of the extracted mitochondria were individually measured by 10-N-alkyl acridine orange and tetramethylrhodamine ethyl ester staining via flow cytometry. Experimental results revealed that expressed pattern of complex I–V in device-extracted mitochondria was close to that of mitochondria in total cell lysis and device extraction significantly prevented chemical modification of complex IV protein via a conventional kit, although device extract similar amounts of mitochondria to the conventional kit revealed by Tom20 expression. Furthermore, purity of device-extracted mitochondria was above 93.7% and mitochondria still retained normal activity after device extraction proven by expression of mitochondrial membrane potential as well as the entire mitochondrial morphology. These results confirmed that the proposed microfluidic device could obtain functional mitochondria without structural damage.
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Sanchez, Victoria, Shawn D. Feinstein, Nadia Lunardi, Pavle M. Joksovic, Annalisa Boscolo, Slobodan M. Todorovic, and Vesna Jevtovic-Todorovic. "General Anesthesia Causes Long-term Impairment of Mitochondrial Morphogenesis and Synaptic Transmission in Developing Rat Brain." Anesthesiology 115, no. 5 (November 1, 2011): 992–1002. http://dx.doi.org/10.1097/aln.0b013e3182303a63.
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Background Clinically used general anesthetics, alone or in combination, are damaging to the developing mammalian brain. In addition to causing widespread apoptotic neurodegeneration in vulnerable brain regions, exposure to general anesthesia at the peak of synaptogenesis causes learning and memory deficiencies later in life. In vivo rodent studies have suggested that activation of the intrinsic (mitochondria-dependent) apoptotic pathway is the earliest warning sign of neuronal damage, suggesting that a disturbance in mitochondrial integrity and function could be the earliest triggering events. Methods Because proper and timely mitochondrial morphogenesis is critical for brain development, the authors examined the long-term effects of a commonly used anesthesia combination (isoflurane, nitrous oxide, and midazolam) on the regional distribution, ultrastructural properties, and electron transport chain function of mitochondria, as well as synaptic neurotransmission, in the subiculum of rat pups. Results This anesthesia, administered at the peak of synaptogenesis, causes protracted injury to mitochondria, including significant enlargement of mitochondria (more than 30%, P < 0.05), impairment of their structural integrity, an approximately 28% increase in their complex IV activity (P < 0.05), and a twofold decrease in their regional distribution in presynaptic neuronal profiles (P < 0.05), where their presence is important for the normal development and functioning of synapses. Consequently, the authors showed that impaired mitochondrial morphogenesis is accompanied by heightened autophagic activity, decrease in mitochondrial density (approximately 27%, P < 0.05), and long-lasting disturbances in inhibitory synaptic neurotransmission. The interrelation of these phenomena remains to be established. Conclusion Developing mitochondria are exquisitely vulnerable to general anesthesia and may be important early target of anesthesia-induced developmental neurodegeneration.
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Harbauer, Angelika B. "Mitochondrial health maintenance in axons." Biochemical Society Transactions 45, no. 5 (August 4, 2017): 1045–52. http://dx.doi.org/10.1042/bst20170023.
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Neurons are post-mitotic cells that must function throughout the life of an organism. The high energetic requirements and Ca2+ spikes of synaptic transmission place a burden on neuronal mitochondria. The removal of older mitochondria and the replenishment of the functional mitochondrial pool in axons with freshly synthesized components are therefore important parts of neuronal maintenance. Although the mechanism of mitochondrial protein import and dynamics is studied in great detail, the length of neurons poses additional challenges to those processes. In this mini-review, I briefly cover the basics of mitochondrial biogenesis and proceed to explain the interdependence of mitochondrial transport and mitochondrial health. I then extrapolate recent findings in yeast and mammalian cultured cells to neurons, making a case for axonal translation as a contributor to mitochondrial biogenesis in neurons.
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Pedersen, H. S., P. Løvendahl, N. K. Nikolaisen, P. Holm, P. Hyttel, J. R. Nyengaard, F. Chen, and H. Callesen. "152 MITOCHONDRIAL DYNAMICS IN PRE- AND POSTPUBERTAL PIG OOCYTES BEFORE AND AFTER IN VITRO MATURATION." Reproduction, Fertility and Development 26, no. 1 (2014): 189. http://dx.doi.org/10.1071/rdv26n1ab152.
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Oocytes from prepubertal (PRE) or postpubertal (POST) pigs are used in, for example, somatic cell nuclear transfer and in vitro fertilization. Here we describe mitochondrial dynamics in pig oocytes of different sizes before and after in vitro maturation (IVM), isolated from PRE or POST animals. In PRE oocytes, inside-zona pellucida diameter was measured before and after IVM (μm; small: ≤110, medium: >110, large: ≥120) and used for evaluation of (1) mitochondrial numbers before maturation and (2) mitochondrial morphology and location before and after maturation in comparison with POST oocytes. Oocytes were processed for transmission electron microscopy (Acta Anat. 129:12). For assessment of mitochondrial numbers, paired dissector sections were collected at uniform intervals throughout the oocyte, and in each set of dissector sections a known area fraction was sampled for mitochondrial counting in physical dissectors (J. Microsc. 134:127). Total number of mitochondria was calculated, and oocyte volume was estimated by Cavalieri estimator (J. Microsc. 147:229). Data were analysed by ANOVA. Mitochondrial morphology was classified as elongated, round, shell-like, or compartmentalized; mitochondrial cristae as transverse or peripheral; and mitochondrial location as cortical, subcortical, or central. Before IVM, small PRE presented elongated and round mitochondria with transverse cristae; medium and large PRE presented round mitochondria with peripheral and transverse cristae; POST presented round mitochondria with peripheral cristae in all cases. After IVM, small and medium PRE had round mitochondria with peripheral cristae; medium PRE and POST had shell-like mitochondria with peripheral cristae; large PRE had compartmentalized mitochondria with peripheral cristae. Before IVM, small PRE displayed cortical mitochondrial location, whereas the location in other groups was cortical and central. After IVM, mitochondria were located centrally in some large PRE and in all POST. Mitochondrial number increased during oocyte growth proportional to the increase in oocyte volume (Table 1). Shell-like and compartmentalized mitochondria indicate (1) dividing mitochondria (increasing mitochondrial numbers during maturation), or (2) apoptosis-related mitochondrial fission (compromised oocytes after maturation). After IVM, mitochondria seemed to reach the final central position most consistently in POST. These differences may partly explain the higher developmental competence in larger PRE and POST oocytes. Table 1.Mitochondrial number and oocyte volume in pre- and postpubertal pigs
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Ouyang, Yi-Bing, and Rona G. Giffard. "ER-Mitochondria Crosstalk during Cerebral Ischemia: Molecular Chaperones and ER-Mitochondrial Calcium Transfer." International Journal of Cell Biology 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/493934.
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It is commonly believed that sustained elevations in the mitochondrial matrix Ca2+concentration are a major feature of the intracellular cascade of lethal events during cerebral ischemia. The physical association between the endoplasmic reticulum (ER) and mitochondria, known as the mitochondria-associated ER membrane (MAM), enables highly efficient transmission of Ca2+from the ER to mitochondria under both physiological and pathological conditions. Molecular chaperones are well known for their protective effects during cerebral ischemia. It has been demonstrated recently that many molecular chaperones coexist with MAM and regulate the MAM and thus Ca2+concentration inside mitochondria. Here, we review recent research on cerebral ischemia and MAM, with a focus on molecular chaperones and ER-mitochondrial calcium transfer.
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Wang, Qiang, Ann M. Ratchford, Maggie M. Y. Chi, Erica Schoeller, Antonina Frolova, Tim Schedl, and Kelle H. Moley. "Maternal Diabetes Causes Mitochondrial Dysfunction and Meiotic Defects in Murine Oocytes." Molecular Endocrinology 23, no. 10 (October 1, 2009): 1603–12. http://dx.doi.org/10.1210/me.2009-0033.
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Abstract The adverse effects of maternal diabetes on embryo development and pregnancy outcomes have recently been shown to occur as early as the one-cell zygote stage. The hypothesis of this study was that maternally inherited mitochondria in oocytes from diabetic mice are abnormal and thus responsible in part for this latency of developmental compromise. In ovulated oocytes from diabetic mice, transmission electron microscopy revealed an alteration in mitochondrial ultrastructure, and the quantitative analysis of mitochondrial DNA copy number demonstrated an increase. The levels of ATP and tricarboxylic acid cycle metabolites in diabetic oocytes were markedly reduced compared with controls, suggesting a mitochondrial metabolic dysfunction. Abnormal distribution of mitochondria within maturing oocytes also was seen in diabetic mice. Furthermore, oocytes from diabetic mice displayed a higher frequency of spindle defects and chromosome misalignment in meiosis, resulting in increased aneuploidy rates in ovulated oocytes. Collectively, our results suggest that maternal diabetes results in oocyte defects that are transmitted to the fetus by two routes: first, meiotic spindle and chromatin defects result in nondisjunction leading to embryonic aneuploidy; second, structural and functional abnormalities of oocyte mitochondria, through maternal transmission, provide the embryo with a dysfunctional complement of mitochondria that may be propagated during embryogenesis.
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Wang, Qiang, Ann M. Ratchford, Maggie M. Y. Chi, Erica Schoeller, Antonina Frolova, Tim Schedl, and Kelle H. Moley. "Maternal Diabetes Causes Mitochondrial Dysfunction and Meiotic Defects in Murine Oocytes." Journal of Clinical Endocrinology & Metabolism 94, no. 9 (September 1, 2009): 3618. http://dx.doi.org/10.1210/jcem.94.9.9995.
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The adverse effects of maternal diabetes on embryo development and pregnancy outcomes have recently been shown to occur as early as the one-cell zygote stage. The hypothesis of this study was that maternally inherited mitochondria in oocytes from diabetic mice are abnormal and thus responsible in part for this latency of developmental compromise. In ovulated oocytes from diabetic mice, transmission electron microscopy revealed an alteration in mitochondrial ultrastructure, and the quantitative analysis of mitochondrial DNA copy number demonstrated an increase. The levels of ATP and tricarboxylic acid cycle metabolites in diabetic oocytes were markedly reduced compared with controls, suggesting a mitochondrial metabolic dysfunction. Abnormal distribution of mitochondria within maturing oocytes also was seen in diabetic mice. Furthermore, oocytes from diabetic mice displayed a higher frequency of spindle defects and chromosome misalignment in meiosis, resulting in increased aneuploidy rates in ovulated oocytes. Collectively, our results suggest that maternal diabetes results in oocyte defects that are transmitted to the fetus by two routes: first, meiotic spindle and chromatin defects result in nondisjunction leading to embryonic aneuploidy; second, structural and functional abnormalities of oocyte mitochondria, through maternal transmission, provide the embryo with a dysfunctional complement of mitochondria that may be propagated during embryogenesis.
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Hobbs, Alyson E. Aiken, Maithreyan Srinivasan, J. Michael McCaffery, and Robert E. Jensen. "Mmm1p, a Mitochondrial Outer Membrane Protein, Is Connected to Mitochondrial DNA (Mtdna) Nucleoids and Required for Mtdna Stability." Journal of Cell Biology 152, no. 2 (January 22, 2001): 401–10. http://dx.doi.org/10.1083/jcb.152.2.401.
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In the yeast Saccharomyces cerevisiae, mitochondria form a branched, tubular reticulum in the periphery of the cell. Mmm1p is required to maintain normal mitochondrial shape and in mmm1 mutants mitochondria form large, spherical organelles. To further explore Mmm1p function, we examined the localization of a Mmm1p–green fluorescent protein (GFP) fusion in living cells. We found that Mmm1p-GFP is located in small, punctate structures on the mitochondrial outer membrane, adjacent to a subset of matrix-localized mitochondrial DNA nucleoids. We also found that the temperature-sensitive mmm1-1 mutant was defective in transmission of mitochondrial DNA to daughter cells immediately after the shift to restrictive temperature. Normal mitochondrial nucleoid structure also collapsed at the nonpermissive temperature with similar kinetics. Moreover, we found that mitochondrial inner membrane structure is dramatically disorganized in mmm1 disruption strains. We propose that Mmm1p is part of a connection between the mitochondrial outer and inner membranes, anchoring mitochondrial DNA nucleoids in the matrix.
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SEN, MADHUMITA, EMILY MCMAINS, and EVANNA GLEASON. "Local influence of mitochondrial calcium transport in retinal amacrine cells." Visual Neuroscience 24, no. 5 (August 16, 2007): 663–78. http://dx.doi.org/10.1017/s0952523807070551.
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Ca2+-dependent synaptic transmission from retinal amacrine cells is thought to be initiated locally at dendritic processes. Hence, understanding the spatial and temporal impact of Ca2+ transport is fundamental to understanding how amacrine cells operate. Here, we provide the first examination of the local effects of mitochondrial Ca2+ transport in neuronal processes. By combining mitochondrial localization with measurements of cytosolic Ca2+, the local impacts of mitochondrial Ca2+ transport for two types of Ca2+ signals were investigated. Disruption of mitochondrial Ca2+ uptake with carbonyl cyanide 4-(trifluoromethoxy) phenylhydrazone (FCCP) produces cytosolic Ca2+ elevations. The amplitudes of these elevations decline with distance from mitochondria suggesting that they are related to mitochondrial Ca2+ transport. The time course of the FCCP-dependent Ca2+ elevations depend on the availability of ER Ca2+ and we provide evidence that Ca2+ is released primarily via nearby ryanodine receptors. These results indicate that interactions between the ER and mitochondria influence cytosolic Ca2+ in amacrine cell processes and cell bodies. We also demonstrate that the durations of glutamate-dependent Ca2+ elevations are dependent on their proximity to mitochondria in amacrine cell processes. Consistent with this observation, disruption of mitochondrial Ca2+ transport alters the duration of glutamate-dependent Ca2+ elevations near mitochondria but not at sites more than 10 μm away. These results indicate that mitochondria influence local Ca2+-dependent signaling in amacrine cell processes.
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Santana-Román, María E., Paola Maycotte, Salvador Uribe-Carvajal, Cristina Uribe-Alvarez, Nayeli Alvarado-Medina, Mohsin Khan, Aleem Siddiqui, and Victoria Pando-Robles. "Monitoring Mitochondrial Function in Aedes albopictus C6/36 Cell Line during Dengue Virus Infection." Insects 12, no. 10 (October 14, 2021): 934. http://dx.doi.org/10.3390/insects12100934.
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Aedes aegypti and Aedes albopictus mosquitoes are responsible for dengue virus (DENV) transmission in tropical and subtropical areas worldwide, where an estimated 3 billion people live at risk of DENV exposure. DENV-infected individuals show symptoms ranging from sub-clinical or mild to hemorrhagic fever. Infected mosquitoes do not show detectable signs of disease, even though the virus maintains a lifelong persistent infection. The interactions between viruses and host mitochondria are crucial for virus replication and pathogenicity. DENV infection in vertebrate cells modulates mitochondrial function and dynamics to facilitate viral proliferation. Here, we describe that DENV also regulates mitochondrial function and morphology in infected C6/36 mosquito cells (derived from Aedes albopictus). Our results showed that DENV infection increased ROS (reactive oxygen species) production, modulated mitochondrial transmembrane potential and induced changes in mitochondrial respiration. Furthermore, we offer the first evidence that DENV causes translocation of mitofusins to mitochondria in the C6/36 mosquito cell line. Another protein Drp-1 (Dynamin-related protein 1) did not localize to mitochondria in DENV-infected cells. This observation therefore ruled out the possibility that the abovementioned alterations in mitochondrial function are associated with mitochondrial fission. In summary, this report provides some key insights into the virus–mitochondria crosstalk in DENV infected mosquito cells.
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Tempio, Alessandra, Mauro Niso, Luna Laera, Lucia Trisolini, Maria Favia, Lucia Ciranna, Domenico Marzulli, et al. "Mitochondrial Membranes of Human SH-SY5Y Neuroblastoma Cells Express Serotonin 5-HT7 Receptor." International Journal of Molecular Sciences 21, no. 24 (December 17, 2020): 9629. http://dx.doi.org/10.3390/ijms21249629.
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Mitochondria in neurons contribute to energy supply, the regulation of synaptic transmission, Ca2+ homeostasis, neuronal excitability, and stress adaptation. In recent years, several studies have highlighted that the neurotransmitter serotonin (5-HT) plays an important role in mitochondrial biogenesis in cortical neurons, and regulates mitochondrial activity and cellular function in cardiomyocytes. 5-HT exerts its diverse actions by binding to cell surface receptors that are classified into seven distinct families (5-HT1 to 5-HT7). Recently, it was shown that 5-HT3 and 5-HT4 receptors are located on the mitochondrial membrane and participate in the regulation of mitochondrial function. Furthermore, it was observed that activation of brain 5-HT7 receptors rescued mitochondrial dysfunction in female mice from two models of Rett syndrome, a rare neurodevelopmental disorder characterized by severe behavioral and physiological symptoms. Our Western blot analyses performed on cell-lysate and purified mitochondria isolated from neuronal cell line SH-SY5Y showed that 5-HT7 receptors are also expressed into mitochondria. Maximal binding capacity (Bmax) obtained by Scatchard analysis on purified mitochondrial membranes was 0.081 pmol/mg of 5-HT7 receptor protein. Lastly, we evaluated the effect of selective 5-HT7 receptor agonist LP-211 and antagonist (inverse agonist) SB-269970 on mitochondrial respiratory chain (MRC) cytochrome c oxidase activity on mitochondria from SH-SY5Y cells. Our findings provide the first evidence that 5-HT7 receptor is also expressed in mitochondria.
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Handa, Hirokazu. "Investigation of the origin and transmission of linear mitochondrial plasmid based on phylogenetic analysis in Japanese rapeseed varieties." Genome 50, no. 2 (February 2007): 234–40. http://dx.doi.org/10.1139/g06-150.
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A linear mitochondrial plasmid is present in some varieties of rapeseed. To elucidate its origin and transmission the author investigated types of mitochondrial genome and the presence of plasmid in 78 rapeseed varieties and landraces in Japan and carried out a comparative analysis using the breeding history of Japanese rapeseed varieties. The mitochondrial genome of rapeseed was classified roughly into 2 types, type I (nap) and type II (cam). Type II rapeseed mitochondria closely resembles that of Brassica rapa , which is a related species of rapeseed. In this study, the author found that all varieties with type II mitochondria originated from interspecific crosses between rapeseed ( B. napus ) and B. rapa. This indicates that type II cytoplasm was introduced to rapeseed through a breeding program. The presence of plasmid was limited to B. rapa landraces and rapeseed varieties that arose by interspecific crosses between B. napus and B. rapa. The results suggest that mitochondrial plasmid is of B. rapa origin and that it has been introduced into rapeseed by interspecific crosses in a modern breeding program, as in the case of the mitochondrial genome. Phylogenetic study of Japanese rapeseed varieties suggests the participation not of the mitochondrial genome but, rather, the nuclear genome for the perpetuation of plasmid in progeny varieties.
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Bertrand, Helmut. "Senescence is coupled to induction of an oxidative phosphorylation stress response by mitochondrial DNA mutations in Neurospora." Canadian Journal of Botany 73, S1 (December 31, 1995): 198–204. http://dx.doi.org/10.1139/b95-246.
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In Neurospora and other genera of filamentous fungi, the occurrence of a mutation affecting one or several genes on the chromosome of a single mitochondrion can trigger the gradual displacement of wild-type mitochondrial DNA by mutant molecules in asexually propagated cultures. As this displacement progresses, the cultures senesce gradually and die if the mitochondrial mutation is lethal, or develop respiratory deficiencies if the mutation is nonlethal. Mitochondrial mutations that elicit the displacement of wild-type mitochondrial DNAs are said to be "suppressive." In the strictly aerobic fungi, suppressiveness appears to be associated exclusively with mutations that diminish cytochrome-mediated mitochondrial redox functions and, thus, curtail oxidative phosphorylation. In Neurospora, suppressiveness is connected to a regulatory system through which cells respond to chemical or genetic insults to the mitochondrial electron-transport system by increasing the number of mitochondria approximately threefold. Mutant alleles of two nuclear genes, osr-1 and osr-2, affect this stress response and abrogate the suppressiveness of mitochondrial mutations. Therefore, we propose that mitochondrial mutations are suppressive because their phenotypic effect is limited to the organelles within which the mutant DNA is located. Consequently, mitochondria that are "homozygous" for a mutant allele are functionally crippled and are induced to proliferate more rapidly than the normal mitochondria with which they coexist in a common protoplasm. While this model provides a plausible explanation for the suppressiveness of mitochondrial mutations in the strictly aerobic fungi, it may not account for the biased transmission of mutant mitochondrial DNAs in the facultatively anaerobic yeasts. Key words: mitochondria, mitochondrial DNA, mutations, suppressiveness, oxidative phosphorylation, stress response.
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Picard, Martin, Kathryn White, and Douglass M. Turnbull. "Mitochondrial morphology, topology, and membrane interactions in skeletal muscle: a quantitative three-dimensional electron microscopy study." Journal of Applied Physiology 114, no. 2 (January 15, 2013): 161–71. http://dx.doi.org/10.1152/japplphysiol.01096.2012.
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Dynamic remodeling of mitochondrial morphology through membrane dynamics are linked to changes in mitochondrial and cellular function. Although mitochondrial membrane fusion/fission events are frequent in cell culture models, whether mitochondrial membranes dynamically interact in postmitotic muscle fibers in vivo remains unclear. Furthermore, a quantitative assessment of mitochondrial morphology in intact muscle is lacking. Here, using electron microscopy (EM), we provide evidence of interacting membranes from adjacent mitochondria in intact mouse skeletal muscle. Electron-dense mitochondrial contact sites consistent with events of outer mitochondrial membrane tethering are also described. These data suggest that mitochondrial membranes interact in vivo among mitochondria, possibly to induce morphology transitions, for kiss-and-run behavior, or other processes involving contact between mitochondrial membranes. Furthermore, a combination of freeze-fracture scanning EM and transmission EM in orthogonal planes was used to characterize and quantify mitochondrial morphology. Two subpopulations of mitochondria were studied: subsarcolemmal (SS) and intermyofibrillar (IMF), which exhibited significant differences in morphological descriptors, including form factor (means ± SD for SS: 1.41 ± 0.45 vs. IMF: 2.89 ± 1.76, P < 0.01) and aspect ratio (1.97 ± 0.83 vs. 3.63 ± 2.13, P < 0.01) and circularity (0.75 ± 0.16 vs. 0.45 ± 0.22, P < 0.01) but not size (0.28 ± 0.31 vs. 0.27 ± 0.20 μm2). Frequency distributions for mitochondrial size and morphological parameters were highly skewed, suggesting the presence of mechanisms to influence mitochondrial size and shape. In addition, physical continuities between SS and IMF mitochondria indicated mixing of both subpopulations. These data provide evidence that mitochondrial membranes interact in vivo in mouse skeletal muscle and that factors may be involved in regulating skeletal muscle mitochondrial morphology.
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Barbieri, Elena, Michela Battistelli, Lucia Casadei, Luciana Vallorani, Giovanni Piccoli, Michele Guescini, Anna Maria Gioacchini, et al. "Morphofunctional and Biochemical Approaches for Studying Mitochondrial Changes during Myoblasts Differentiation." Journal of Aging Research 2011 (2011): 1–16. http://dx.doi.org/10.4061/2011/845379.
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This study describes mitochondrial behaviour during the C2C12 myoblast differentiation program and proposes a proteomic approach to mitochondria integrated with classical morphofunctional and biochemical analyses. Mitochondrial ultrastructure variations were determined by transmission electron microscopy; mitochondrial mass and membrane potential were analysed by Mitotracker Green and JC-1 stains and by epifluorescence microscope. Expression ofPGC1,NRF1andTfamgenes controlling mitochondrial biogenesis was studied by real-time PCR. The mitochondrial functionality was tested by cytochrome c oxidase activity andCOXIIexpression. Mitochondrial proteomic profile was also performed. These assays showed that mitochondrial biogenesis and activity significantly increase in differentiating myotubes. The proteomic profile identifies 32 differentially expressed proteins, mostly involved in oxidative metabolism, typical of myotubes formation. Other notable proteins, such as superoxide dismutase (MnSOD), a cell protection molecule, and voltage-dependent anion-selective channel protein (VDAC1) involved in the mitochondria-mediated apoptosis, were found to be regulated by the myogenic process. The integration of these approaches represents a helpful tool for studying mitochondrial dynamics, biogenesis, and functionality in comparative surveys on mitochondrial pathogenic or senescent satellite cells.
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Zhong, Zhisheng, Yanhong Hao, Rongfeng Li, Lee Spate, David Wax, Qing-Yuan Sun, Randall S. Prather, and Heide Schatten. "Analysis of Heterogeneous Mitochondria Distribution in Somatic Cell Nuclear Transfer Porcine Embryos." Microscopy and Microanalysis 14, no. 5 (September 16, 2008): 418–32. http://dx.doi.org/10.1017/s1431927608080896.
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AbstractWe previously reported that translocation of mitochondria from the oocyte cortex to the perinuclear area indicates positive developmental potential that was reduced in porcine somatic cell nuclear transfer (SCNT) embryos compared to in vitro–fertilized (IVF) embryos (Katayama, M., Zhong, Z.-S., Lai, L., Sutovsky, P., Prather, R.S. & Schatten, H. (2006). Dev Biol299, 206–220.). The present study is focused on distribution of donor cell mitochondria in intraspecies (pig oocytes; pig fetal fibroblast cells) and interspecies (pig oocytes; mouse fibroblast cells) reconstructed embryos by using either pig fibroblasts with mitochondria-stained MitoTracker CMXRos or YFP-mitochondria 3T3 cells (pPhi-Yellow-mito) as donor cells. Transmission electron microscopy was employed for ultrastructural analysis of pig oocyte and donor cell mitochondria. Our results revealed donor cell mitochondrial clusters around the donor nucleus that gradually dispersed into the ooplasm at 3 h after SCNT. Donor-derived mitochondria distributed into daughter blastomeres equally (82.8%) or unequally (17.2%) at first cleavage. Mitochondrial morphology was clearly different between donor cells and oocytes in which various complex shapes and configurations were seen. These data indicate that (1) unequal donor cell mitochondria distribution is observed in 17.2% of embryos, which may negatively influence development; and (2) complex mitochondrial morphologies are observed in IVF and SCNT embryos, which may influence mitochondrial translocation and affect development.
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Reunov, Arkadiy A., and Yulia A. Reunova. "Pre-meiotic transformation of germplasm-related structures during male gamete differentiation in Xenopus laevis." Zygote 24, no. 1 (December 16, 2014): 42–47. http://dx.doi.org/10.1017/s0967199414000690.
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SummaryTo highlight the ultrastructural features of transformation occurring with germplasm-related structures (GPRS), the spermatogenic cells of Xenopus laevis were studied by transmission electron microscopy and quantitative analysis. It was determined that in spermatogonia and spermatocytes, the compact germinal granules underwent fragmentation into particles comparable with inter-mitochondrial cement (IMC). Fragments of IMC agglutinated some cell mitochondria and resulted in the creation of mitochondrial clusters. Clustered mitochondria responded with loss of their membranes that occurred by the twisting of membranous protrusions around themselves until multi-layered membranes were formed. The mitochondrial affinity of multi-layered membranes was proven by an immunopositive test for mitochondrial dihydrolipoamide acetyltransferase. As a consequence of mitochondrial membrane twisting, the naked mitochondrial cores appeared and presumably underwent dispersion, which is the terminal stage of GPRS transformation. As no GPRS were observed in spermatids and sperm, it was assumed that these structures are functionally assigned to early stages of meiotic differentiation.
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Lujan, Brendan, Christopher Kushmerick, Tania Das Banerjee, Ruben K. Dagda, and Robert Renden. "Glycolysis selectively shapes the presynaptic action potential waveform." Journal of Neurophysiology 116, no. 6 (December 1, 2016): 2523–40. http://dx.doi.org/10.1152/jn.00629.2016.
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Mitochondria are major suppliers of cellular energy in neurons; however, utilization of energy from glycolysis vs. mitochondrial oxidative phosphorylation (OxPhos) in the presynaptic compartment during neurotransmission is largely unknown. Using presynaptic and postsynaptic recordings from the mouse calyx of Held, we examined the effect of acute selective pharmacological inhibition of glycolysis or mitochondrial OxPhos on multiple mechanisms regulating presynaptic function. Inhibition of glycolysis via glucose depletion and iodoacetic acid (1 mM) treatment, but not mitochondrial OxPhos, rapidly altered transmission, resulting in highly variable, oscillating responses. At reduced temperature, this same treatment attenuated synaptic transmission because of a smaller and broader presynaptic action potential (AP) waveform. We show via experimental manipulation and ion channel modeling that the altered AP waveform results in smaller Ca2+ influx, resulting in attenuated excitatory postsynaptic currents (EPSCs). In contrast, inhibition of mitochondria-derived ATP production via extracellular pyruvate depletion and bath-applied oligomycin (1 μM) had no significant effect on Ca2+ influx and did not alter the AP waveform within the same time frame (up to 30 min), and the resultant EPSC remained unaffected. Glycolysis, but not mitochondrial OxPhos, is thus required to maintain basal synaptic transmission at the presynaptic terminal. We propose that glycolytic enzymes are closely apposed to ATP-dependent ion pumps on the presynaptic membrane. Our results indicate a novel mechanism for the effect of hypoglycemia on neurotransmission. Attenuated transmission likely results from a single presynaptic mechanism at reduced temperature: a slower, smaller AP, before and independent of any effect on synaptic vesicle release or receptor activity.
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Castro-Sepulveda, Mauricio, Sebastian Jannas-Vela, Rodrigo Fernández-Verdejo, Daniela Ávalos-Allele, German Tapia, Claudio Villagrán, Nicolas Quezada, and Hermann Zbinden-Foncea. "Relative lipid oxidation associates directly with mitochondrial fusion phenotype and mitochondria-sarcoplasmic reticulum interactions in human skeletal muscle." American Journal of Physiology-Endocrinology and Metabolism 318, no. 6 (June 1, 2020): E848—E855. http://dx.doi.org/10.1152/ajpendo.00025.2020.
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Disturbances in skeletal muscle lipid oxidation might induce ectopic fat deposition and lipotoxicity. Nevertheless, the cellular mechanisms that regulate skeletal muscle lipid oxidation have not been fully determined. We aimed to determine whether there was an association between relative whole body lipid oxidation and mitochondrial size or mitochondria-sarcoplasmic reticulum interactions in the skeletal muscle. Twelve healthy men were included [mean (standard deviation), 24.7 (1.5) yr old, 24.4 (2.6) kg/m2]. The respiratory quotient (RQ) was used to estimate relative lipid oxidation at rest and during exercise (50% maximal oxygen consumption, 600 kcal expended). A skeletal muscle biopsy was obtained from the vastus lateralis at rest. Transmission electron microscopy was used to determine mitochondrial size and mitochondria-sarcoplasmic reticulum interactions (≤50 nm of distance between organelles). Protein levels of fusion/fission regulators were measured in skeletal muscle by Western blot. Resting RQ and exercise RQ associated inversely with intermyofibrillar mitochondrial size ( r = −0.66 and r = −0.60, respectively, P < 0.05). Resting RQ also associated inversely with the percentage of intermyofibrillar mitochondria-sarcoplasmic reticulum interactions ( r = −0.62, P = 0.03). Finally, intermyofibrillar mitochondrial size associated inversely with lipid droplet density ( r = −0.66, P = 0.01) but directly with mitochondria fusion-to-fission ratio ( r = 0.61, P = 0.03). Our results show that whole body lipid oxidation is associated with skeletal muscle intermyofibrillar mitochondrial size, fusion phenotype, and mitochondria-sarcoplasmic-reticulum interactions in nondiabetic humans.
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Faustini, Gaia, Elena Marchesan, Laura Zonta, Federica Bono, Emanuela Bottani, Francesca Longhena, Elena Ziviani, Alessandra Valerio, and Arianna Bellucci. "Alpha-Synuclein Preserves Mitochondrial Fusion and Function in Neuronal Cells." Oxidative Medicine and Cellular Longevity 2019 (November 23, 2019): 1–11. http://dx.doi.org/10.1155/2019/4246350.
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Dysregulations of mitochondria with alterations in trafficking and morphology of these organelles have been related to Parkinson’s disease (PD), a neurodegenerative disorder characterized by brain accumulation of Lewy bodies (LB), intraneuronal inclusions mainly composed of α-synuclein (α-syn) fibrils. Experimental evidence supports that α-syn pathological aggregation can negatively impinge on mitochondrial functions suggesting that this protein may be crucially involved in the control of mitochondrial homeostasis. The aim of this study was to assay this hypothesis by analyzing mitochondrial function and morphology in primary cortical neurons from C57BL/6JOlaHsd α-syn null and C57BL/6J wild-type (wt) mice. Primary cortical neurons from mice lacking α-syn showed decreased respiration capacity measured with a Seahorse XFe24 Extracellular Flux Analyzer. In addition, morphological Airyscan superresolution microscopy showed the presence of fragmented mitochondria while real-time PCR and western blot confirmed altered expression of proteins involved in mitochondrial shape modifications in the primary cortical neurons of α-syn null mice. Transmission electron microscopy (TEM) studies showed that α-syn null neurons exhibited impaired mitochondria-endoplasmic reticulum (ER) physical interaction. Specifically, we identified a decreased number of mitochondria-ER contacts (MERCs) paralleled by a significant increase in ER-mitochondria distance (i.e., MERC length). These findings support that α-syn physiologically preserves mitochondrial functions and homeostasis. Studying α-syn/mitochondria interplay in health and disease is thus pivotal for understanding their involvement in PD and other LB disorders.
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Zhou, Zeyu, Jocelyn Vidales, José A. González-Reyes, Bradley Shibata, Keith Baar, Jennifer M. Rutkowsky, and Jon J. Ramsey. "A 1-Month Ketogenic Diet Increased Mitochondrial Mass in Red Gastrocnemius Muscle, but Not in the Brain or Liver of Middle-Aged Mice." Nutrients 13, no. 8 (July 24, 2021): 2533. http://dx.doi.org/10.3390/nu13082533.
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Alterations in markers of mitochondrial content with ketogenic diets (KD) have been reported in tissues of rodents, but morphological quantification of mitochondrial mass using transmission electron microscopy (TEM), the gold standard for mitochondrial quantification, is needed to further validate these findings and look at specific regions of interest within a tissue. In this study, red gastrocnemius muscle, the prefrontal cortex, the hippocampus, and the liver left lobe were used to investigate the impact of a 1-month KD on mitochondrial content in healthy middle-aged mice. The results showed that in red gastrocnemius muscle, the fractional area of both subsarcolemmal (SSM) and intermyofibrillar (IMM) mitochondria was increased, and this was driven by an increase in the number of mitochondria. Mitochondrial fractional area or number was not altered in the liver, prefrontal cortex, or hippocampus following 1 month of a KD. These results demonstrate tissue-specific changes in mitochondrial mass with a short-term KD and highlight the need to study different muscle groups or tissue regions with TEM to thoroughly determine the effects of a KD on mitochondrial mass.
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García-Pérez, Cecília, Timothy G. Schneider, György Hajnóczky, and György Csordás. "Alignment of sarcoplasmic reticulum-mitochondrial junctions with mitochondrial contact points." American Journal of Physiology-Heart and Circulatory Physiology 301, no. 5 (November 2011): H1907—H1915. http://dx.doi.org/10.1152/ajpheart.00397.2011.
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Propagation of ryanodine receptor (RyR2)-derived Ca2+ signals to the mitochondrial matrix supports oxidative ATP production or facilitates mitochondrial apoptosis in cardiac muscle. Ca2+ transfer likely occurs locally at focal associations of the sarcoplasmic reticulum (SR) and mitochondria, which are secured by tethers. The outer mitochondrial membrane and inner mitochondrial membrane (OMM and IMM, respectively) also form tight focal contacts (contact points) that are enriched in voltage-dependent anion channels, the gates of OMM for Ca2+. Contact points could offer the shortest Ca2+ transfer route to the matrix; however, their alignment with the SR-OMM associations remains unclear. Here, in rat heart we have studied the distribution of mitochondria-associated SR in submitochondrial membrane fractions and evaluated the colocalization of SR-OMM associations with contact points using transmission electron microscopy. In a sucrose gradient designed for OMM purification, biochemical assays revealed lighter fractions enriched in OMM only and heavier fractions containing OMM, IMM, and SR markers. Pure OMM fractions were enriched in mitofusin 2, an ∼80 kDa mitochondrial fusion protein and SR-mitochondrial tether candidate, whereas in fractions of OMM + IMM + SR, a lighter (∼50 kDa) band detected by antibodies raised against the NH2 terminus of mitofusin 2 was dominating. Transmission electron microscopy revealed mandatory presence of contact points at the junctional SR-mitochondrial interface versus a random presence along matching SR-free OMM segments. For each SR-mitochondrial junction at least one tether was attached to contact points. These data establish the contact points as anchorage sites for the SR-mitochondrial physical coupling. Close coupling of the SR, OMM, and IMM is likely to provide a favorable spatial arrangement for local ryanodine receptor-mitochondrial Ca2+ signaling.
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Smith, M. L., L. C. Duchesne, J. N. Bruhn, and J. B. Anderson. "Mitochondrial genetics in a natural population of the plant pathogen armillaria." Genetics 126, no. 3 (November 1, 1990): 575–82. http://dx.doi.org/10.1093/genetics/126.3.575.
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Abstract Transmission and propagation of mitochondrial genotypes in fungi have not been previously investigated in the field. This study examined the distribution of nuclear and mitochondrial genotypes in a natural, local population of the fungal (Basidiomycetes) root-rot pathogen, Armillaria. Six vegetative clones, ranging in size up to 635 m, were identified on the basis of mating-type alleles. Mitochondrial DNA (mtDNA) restriction fragment patterns indicated that each vegetative clone has one, unique mtDNA type. However, as in other basidiomycetous fungi, biparental transmission of mitochondria following laboratory matings of sexually compatible haploid isolates of Armillaria resulted in a uniformly diploid mycelium that was a mosaic for both parental mitochondrial types. Therefore, either matings between monosporous, haploid isolates are uncommon in nature, or when mating does occur, cytoplasmic markers of one partner predominate during subsequent vegetative growth.
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Ferey, Jeremie L. A., Anna L. Boudoures, Michaela Reid, Andrea Drury, Suzanne Scheaffer, Zeel Modi, Attila Kovacs, et al. "A maternal high-fat, high-sucrose diet induces transgenerational cardiac mitochondrial dysfunction independently of maternal mitochondrial inheritance." American Journal of Physiology-Heart and Circulatory Physiology 316, no. 5 (May 1, 2019): H1202—H1210. http://dx.doi.org/10.1152/ajpheart.00013.2019.
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Maternal obesity is correlated with cardiovascular disease in offspring, with a 1.3-fold increase in events observed in offspring of obese women. We have observed that obesity-exposed oocytes demonstrate impaired mitophagy and transmit damaged mitochondria to the offspring. Accordingly, we hypothesized that maternal obesity induces cardiac mitochondrial dysfunction in the offspring via transgenerational inheritance of abnormal oocyte mitochondria. We mated female mice fed a high-fat/high-sucrose (HFS) diet (or chow) with chow-fed males and assessed cardiac structure and function in their descendants that were chow fed in each generation. All F1 to F3 descendants bred via the female in each generation were nonobese and demonstrated cardiac mitochondrial abnormalities with crystal rarefaction and reduced oxygen consumption pointing to a transgenerational effect, while obese F0 dams’ hearts were unaffected. Furthermore, male offspring from F1 to F3 generations and female F1 and F2 offspring developed increased left ventricular (LV) mass (vs. chow-fed controls). Increased LV mass was also observed in offspring generated by in vitro fertilization of obesity-exposed oocytes and gestation in nonobese surrogates, ruling out a gestational environment effect. Contrary to our hypothesis, male F1 also transmitted these effects to their offspring, ruling out maternal mitochondria as the primary mode of transmission. We conclude that transmission of obesity-induced effects in the oocyte nucleus rather than abnormal mitochondria underlie transgenerational inheritance of cardiac mitochondrial defects in descendants of obese females. These findings will spur exploration of epigenetic alterations in the oocyte genome as potential mechanisms whereby a family history of maternal obesity predisposes to cardiovascular disease in humans. Listen to this article's corresponding podcast at https://ajpheart.podbean.com/e/maternal-obesity-induces-transgenerational-cardiac-mitochondrial-dysfunction/ .
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Tworzydlo, Waclaw, Malgorzata Sekula, and Szczepan M. Bilinski. "Transmission of Functional, Wild-Type Mitochondria and the Fittest mtDNA to the Next Generation: Bottleneck Phenomenon, Balbiani Body, and Mitophagy." Genes 11, no. 1 (January 16, 2020): 104. http://dx.doi.org/10.3390/genes11010104.
Full textAbstract:
The most important role of mitochondria is to supply cells with metabolic energy in the form of adenosine triphosphate (ATP). As synthesis of ATP molecules is accompanied by the generation of reactive oxygen species (ROS), mitochondrial DNA (mtDNA) is highly vulnerable to impairment and, consequently, accumulation of deleterious mutations. In most animals, mitochondria are transmitted to the next generation maternally, i.e., exclusively from female germline cells (oocytes and eggs). It has been suggested, in this context, that a specialized mechanism must operate in the developing oocytes enabling escape from the impairment and subsequent transmission of accurate (devoid of mutations) mtDNA from one generation to the next. Literature survey suggest that two distinct and irreplaceable pathways of mitochondria transmission may be operational in various animal lineages. In some taxa, the mitochondria are apparently selected: functional mitochondria with high inner membrane potential are transferred to the cells of the embryo, whereas those with low membrane potential (overloaded with mutations in mtDNA) are eliminated by mitophagy. In other species, the respiratory activity of germline mitochondria is suppressed and ROS production alleviated leading to the same final effect, i.e., transmission of undamaged mitochondria to offspring, via an entirely different route.
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Mignerot, Laure, Chikako Nagasato, Akira F. Peters, Marie-Mathilde Perrineau, Delphine Scornet, Florian Pontheaux, Walid Djema, et al. "Unusual Patterns of Mitochondrial Inheritance in the Brown Alga Ectocarpus." Molecular Biology and Evolution 36, no. 12 (August 20, 2019): 2778–89. http://dx.doi.org/10.1093/molbev/msz186.
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Abstract Most eukaryotes inherit their mitochondria from only one of their parents. When there are different sexes, it is almost always the maternal mitochondria that are transmitted. Indeed, maternal uniparental inheritance has been reported for the brown alga Ectocarpus but we show in this study that different strains of Ectocarpus can exhibit different patterns of inheritance: Ectocarpus siliculosus strains showed maternal uniparental inheritance, as expected, but crosses using different Ectocarpus species 7 strains exhibited either paternal uniparental inheritance or an unusual pattern of transmission where progeny inherited either maternal or paternal mitochondria, but not both. A possible correlation between the pattern of mitochondrial inheritance and male gamete parthenogenesis was investigated. Moreover, in contrast to observations in the green lineage, we did not detect any change in the pattern of mitochondrial inheritance in mutant strains affected in life cycle progression. Finally, an analysis of field-isolated strains provided evidence of mitochondrial genome recombination in both Ectocarpus species.
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Temelie, Mihaela, Diana Iulia Savu, and Nicoleta Moisoi. "Intracellular and Intercellular Signalling Mechanisms following DNA Damage Are Modulated By PINK1." Oxidative Medicine and Cellular Longevity 2018 (June 27, 2018): 1–15. http://dx.doi.org/10.1155/2018/1391387.
Full textAbstract:
Impaired mitochondrial function and accumulation of DNA damage have been recognized as hallmarks of age-related diseases. Mitochondrial dysfunction initiates protective signalling mechanisms coordinated at nuclear level particularly by modulating transcription of stress signalling factors. In turn, cellular response to DNA lesions comprises a series of interconnected complex protective pathways, which require the energetic and metabolic support of the mitochondria. These are involved in intracellular as well as in extracellular signalling of damage. Here, we have initiated a study that addresses how mitochondria-nucleus communication may occur in conditions of combined mitochondrial dysfunction and genotoxic stress and what are the consequences of this interaction on the cell system. In this work, we used cells deficient for PINK1, a mitochondrial kinase involved in mitochondrial quality control whose loss of function leads to the accumulation of dysfunctional mitochondria, challenged with inducers of DNA damage, namely, ionizing radiation and the radiomimetic bleomycin. Combined stress at the level of mitochondria and the nucleus impairs both mitochondrial and nuclear functions. Our findings revealed exacerbated sensibility to genotoxic stress in PINK1-deficient cells. The same cells showed an impaired induction of bystander phenomena following stress insults. However, these cells responded adaptively when a challenge dose was applied subsequently to a low-dose treatment to the cells. The data demonstrates that PINK1 modulates intracellular and intercellular signalling pathways, particularly adaptive responses and transmission of bystander signalling, two facets of the cell-protective mechanisms against detrimental agents.
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Dubinin, Mikhail V., Vlada S. Starinets, Eugeny Yu Talanov, Irina B. Mikheeva, Natalia V. Belosludtseva, Dmitriy A. Serov, Kirill S. Tenkov, Evgeniya V. Belosludtseva, and Konstantin N. Belosludtsev. "Effect of the Non-Immunosuppressive MPT Pore Inhibitor Alisporivir on the Functioning of Heart Mitochondria in Dystrophin-Deficient mdx Mice." Biomedicines 9, no. 9 (September 16, 2021): 1232. http://dx.doi.org/10.3390/biomedicines9091232.
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Supporting mitochondrial function is one of the therapeutic strategies that improve the functioning of skeletal muscle in Duchenne muscular dystrophy (DMD). In this work, we studied the effect of a non-immunosuppressive inhibitor of mitochondrial permeability transition pore (MPTP) alisporivir (5 mg/kg/day), reducing the intensity of the necrotic process and inflammation in skeletal muscles on the cardiac phenotype of dystrophin-deficient mdx mice. We found that the heart mitochondria of mdx mice show an increase in the intensity of oxidative phosphorylation and an increase in the resistance of organelles to the MPT pore opening. Alisporivir had no significant effect on the hyperfunctionalization of the heart mitochondria of mdx mice, and the state of the heart mitochondria of wild-type animals did not affect the dynamics of organelles but significantly suppressed mitochondrial biogenesis and reduced the amount of mtDNA in the heart muscle. Moreover, alisporivir suppressed mitochondrial biogenesis in the heart of wild-type mice. Alisporivir treatment resulted in a decrease in heart weight in mdx mice, which was associated with a significant modification of the transmission of excitation in the heart. The latter was also noted in the case of WT mice treated with alisporivir. The paper discusses the prospects for using alisporivir to correct the function of heart mitochondria in DMD.
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Hintz, W., J. B. Anderson, and P. A. Horgen. "Nuclear migration and mitochondrial inheritance in the mushroom agaricus bitorquis." Genetics 119, no. 1 (May 1, 1988): 35–41. http://dx.doi.org/10.1093/genetics/119.1.35.
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Abstract Mitochondrial (mt) DNA restriction fragment length polymorphisms (RFLPs) were used as genetic markers for following mitochondrial inheritance in the mushroom Agaricus bitorquis. In many basidiomycetes, bilateral nuclear migration between paired homokaryotic mycelia gives rise to two discrete dikaryons which have identical nuclei but different cytoplasms. Although nuclear migration is rare in A. bitorquis, unidirectional nuclear migration occurred when a nuclear donating strain (8-1), was paired with a nuclear recipient strain (34-2). The dikaryon recovered over the nuclear recipient mate (Dik D) contained nuclei from both parents but only mitochondria from the recipient mate; thus nuclei of 8-1, but not mitochondria, migrated through the resident hyphae of 34-2 following hyphal anastomosis. The two mitochondrial types present in a dikaryon recovered at the junction of the two cultures (Dik A) segregated during vegetative growth. Dikaryotic cells having the 34-2 mitochondrial type grew faster than cells with the 8-1 mitochondrial type. Fruitbodies, derived from a mixed population of cells having the same nuclear components but different cytoplasms, were chimeric for mitochondrial type. The transmission of mitochondria was biased in favor of the 8-1 type in the spore progeny of the chimeric fruitbody. Protoplasts of dikaryon (Dik D), which contained both nuclear types but only the 34-2 mitochondrial type, were regenerated and homokaryons containing the 8-1 nuclear type and the 34-2 mitochondrial type were recovered.
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Che, Ruochen, Chunhua Zhu, Guixia Ding, Min Zhao, Mi Bai, Zhanjun Jia, Aihua Zhang, and Songming Huang. "Huaier Cream Protects against Adriamycin-Induced Nephropathy by Restoring Mitochondrial Function via PGC-1αUpregulation." PPAR Research 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/720383.
Full textAbstract:
The mechanism by which Huaier, a Chinese traditional medicine, protects podocytes remains unclear. We designed the present study to examine whether mitochondrial function restored by PGC-1αserves as the major target of Huaier cream in protecting ADR nephropathy. After ADR administration, the podocytes exhibited remarkable cell injury and mitochondrial dysfunction. Additionally, ADR also reduced PGC-1αbothin vivoandin vitro. Following the Huaier treatment, the notable downregulation of PGC-1αand its downstream molecule mitochondrial transcription factor A (TFAM) were almost entirely blocked. Correspondingly, Huaier markedly ameliorated ADR-induced podocyte injury and mitochondrial dysfunction in both rat kidneys and incubated cells as it inhibited the decrease of nephrin and podocin expression, mtDNA copy number, MMP, and ATP content. Transmission electron microscopy result also showed that Huaier protected mitochondria against ADR-induced severe mitophagy and abnormal changes of ultrastructural morphology. In conclusion, Huaier can protect podocytes against ADR-induced cytotoxicity possibly by reversing the dysfunction of mitochondria via PGC-1αoverexpression, which may be a novel therapeutic drug target in glomerular diseases.
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Yamada, Mitsutoshi, Kazuhiro Akashi, Reina Ooka, Kenji Miyado, and Hidenori Akutsu. "Mitochondrial Genetic Drift after Nuclear Transfer in Oocytes." International Journal of Molecular Sciences 21, no. 16 (August 16, 2020): 5880. http://dx.doi.org/10.3390/ijms21165880.
Full textAbstract:
Mitochondria are energy-producing intracellular organelles containing their own genetic material in the form of mitochondrial DNA (mtDNA), which codes for proteins and RNAs essential for mitochondrial function. Some mtDNA mutations can cause mitochondria-related diseases. Mitochondrial diseases are a heterogeneous group of inherited disorders with no cure, in which mutated mtDNA is passed from mothers to offspring via maternal egg cytoplasm. Mitochondrial replacement (MR) is a genome transfer technology in which mtDNA carrying disease-related mutations is replaced by presumably disease-free mtDNA. This therapy aims at preventing the transmission of known disease-causing mitochondria to the next generation. Here, a proof of concept for the specific removal or editing of mtDNA disease-related mutations by genome editing is introduced. Although the amount of mtDNA carryover introduced into human oocytes during nuclear transfer is low, the safety of mtDNA heteroplasmy remains a concern. This is particularly true regarding donor-recipient mtDNA mismatch (mtDNA–mtDNA), mtDNA-nuclear DNA (nDNA) mismatch caused by mixing recipient nDNA with donor mtDNA, and mtDNA replicative segregation. These conditions can lead to mtDNA genetic drift and reversion to the original genotype. In this review, we address the current state of knowledge regarding nuclear transplantation for preventing the inheritance of mitochondrial diseases.
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Leduc-Gaudet, Jean-Philippe, Dominique Mayaki, Olivier Reynaud, Felipe E. Broering, Tomer J. Chaffer, Sabah N. A. Hussain, and Gilles Gouspillou. "Parkin Overexpression Attenuates Sepsis-Induced Muscle Wasting." Cells 9, no. 6 (June 11, 2020): 1454. http://dx.doi.org/10.3390/cells9061454.
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Sepsis elicits skeletal muscle weakness and fiber atrophy. The accumulation of injured mitochondria and depressed mitochondrial functions are considered as important triggers of sepsis-induced muscle atrophy. It is unclear whether mitochondrial dysfunctions in septic muscles are due to the inadequate activation of quality control processes. We hypothesized that overexpressing Parkin, a protein responsible for the recycling of dysfunctional mitochondria by the autophagy pathway (mitophagy), would confer protection against sepsis-induced muscle atrophy by improving mitochondrial quality and content. Parkin was overexpressed for four weeks in the limb muscles of four-week old mice using intramuscular injections of adeno-associated viruses (AAVs). The cecal ligation and perforation (CLP) procedure was used to induce sepsis. Sham operated animals were used as controls. All animals were studied for 48 h post CLP. Sepsis resulted in major body weight loss and myofiber atrophy. Parkin overexpression prevented myofiber atrophy in CLP mice. Quantitative two-dimensional transmission electron microscopy revealed that sepsis is associated with the accumulation of enlarged and complex mitochondria, an effect which was attenuated by Parkin overexpression. Parkin overexpression also prevented a sepsis-induced decrease in the content of mitochondrial subunits of NADH dehydrogenase and cytochrome C oxidase. We conclude that Parkin overexpression prevents sepsis-induced skeletal muscle atrophy, likely by improving mitochondrial quality and contents.
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Jiang, Yuan, Albert Wingnang Leung, Junyan Xiang, and Chuanshan Xu. "LED Light-Activated Hypocrellin B Induces Mitochondrial Damage of Ovarian Cancer Cells." International Journal of Photoenergy 2012 (2012): 1–5. http://dx.doi.org/10.1155/2012/186752.
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Objective. Hypocrellin is a natural photosensitizer from a traditional Chinese herb. In the present study, our aim is to investigate the effect of LED light-activated hypocrellin B on mitochondria of ovarian cancer cells.Material and Methods. Ovarian cancer HO-8910 cells were incubated with hypocrellin B at the concentration of 2.5 μM for 5 h and then irradiated by blue light from a novel LED source. Cell survival rate of HO-8910 cells was measured using MTT assay 24 h after photodynamic treatment of hypocrellin B. Mitochondrial morphology was observed using transmission electron microscopy (TEM). Mitochondrial membrane potential was measured using flow cytometry with JC-1 staining.Results. MTT assay showed that cell survival rate of HO-8910 cells in the photodynamic treatment group has significantly decreased down to27.22±1.26% (P<0.01). Light irradiation alone or hypocrellin B alone showed no significant impact. In our TEM mitochondria of the cells after photodynamic treatment of hypocrellin B showed severe damage with swollen mitochondria that had nearly nonexistant cristae. Mitochondrial membrane potential remarkably decreased after photodynamic action of hypocrellin B.Conclusion. The findings demonstrated that photodynamic action of hypocrellin B significantly decreased cell proliferation of ovarian cancer HO-8910 cells, caused severe damage to mitochondrial structure, and induced mitochondrial membrane collapse.
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Zarrouk, Amira, Anne Vejux, Thomas Nury, Hammam I. El Hajj, Madouda Haddad, Mustapha Cherkaoui-Malki, Jean-Marc Riedinger, Mohamed Hammami, and Gérard Lizard. "Induction of Mitochondrial Changes Associated with Oxidative Stress on Very Long Chain Fatty Acids (C22:0, C24:0, or C26:0)-Treated Human Neuronal Cells (SK-NB-E)." Oxidative Medicine and Cellular Longevity 2012 (2012): 1–15. http://dx.doi.org/10.1155/2012/623257.
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In Alzheimer's disease, lipid alterations point towards peroxisomal dysfunctions. Indeed, a cortical accumulation of saturated very long chain fatty acids (VLCFAs: C22:0, C24:0, C26:0), substrates for peroxisomalβ-oxidation, has been found in Alzheimer patients. This study was realized to investigate the effects of VLCFAs at the mitochondrial level since mitochondrial dysfunctions play crucial roles in neurodegeneration. On human neuronal SK-NB-E cells treated with C22:0, C24:0, or C26:0 (0.1–20 μM; 48 h), an inhibition of cell growth and mitochondrial dysfunctions were observed by cell counting with trypan blue, MTT assay, and measurement of mitochondrial transmembrane potential (Δψm) with DiOC6(3). A stimulation of oxidative stress was observed with DHE and MitoSOX used to quantify superoxide anion production on whole cells and at the mitochondrial level, respectively. With C24:0 and C26:0, by Western blotting, lower levels of mitochondrial complexes III and IV were detected. After staining with MitoTracker and by transmission electron microscopy used to study mitochondrial topography, mass and morphology, major changes were detected in VLCFAs treated-cells: modification of the cytoplasmic distribution of mitochondria, presence of large mitochondria, enhancement of the mitochondrial mass. Thus, VLCFAs can be potential risk factors contributing to neurodegeneration by inducing neuronal damages via mitochondrial dysfunctions.
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Faria-Pereira, Andreia, and Vanessa A. Morais. "Synapses: The Brain’s Energy-Demanding Sites." International Journal of Molecular Sciences 23, no. 7 (March 26, 2022): 3627. http://dx.doi.org/10.3390/ijms23073627.
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The brain is one of the most energy-consuming organs in the mammalian body, and synaptic transmission is one of the major contributors. To meet these energetic requirements, the brain primarily uses glucose, which can be metabolized through glycolysis and/or mitochondrial oxidative phosphorylation. The relevance of these two energy production pathways in fulfilling energy at presynaptic terminals has been the subject of recent studies. In this review, we dissect the balance of glycolysis and oxidative phosphorylation to meet synaptic energy demands in both resting and stimulation conditions. Besides ATP output needs, mitochondria at synapse are also important for calcium buffering and regulation of reactive oxygen species. These two mitochondrial-associated pathways, once hampered, impact negatively on neuronal homeostasis and synaptic activity. Therefore, as mitochondria assume a critical role in synaptic homeostasis, it is becoming evident that the synaptic mitochondria population possesses a distinct functional fingerprint compared to other brain mitochondria. Ultimately, dysregulation of synaptic bioenergetics through glycolytic and mitochondrial dysfunctions is increasingly implicated in neurodegenerative disorders, as one of the first hallmarks in several of these diseases are synaptic energy deficits, followed by synapse degeneration.
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Štětina, T., L. E. Des Marteaux, and V. Koštál. "Insect mitochondria as targets of freezing-induced injury." Proceedings of the Royal Society B: Biological Sciences 287, no. 1931 (July 22, 2020): 20201273. http://dx.doi.org/10.1098/rspb.2020.1273.
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Many insects survive internal freezing, but the great complexity of freezing stress hinders progress in understanding the ultimate nature of freezing-induced injury. Here, we use larvae of the drosophilid fly, Chymomyza costata to assess the role of mitochondrial responses to freezing stress. Respiration analysis revealed that fat body mitochondria of the freeze-sensitive (non-diapause) phenotype significantly decrease oxygen consumption upon lethal freezing stress, while mitochondria of the freeze-tolerant (diapausing, cold-acclimated) phenotype do not lose respiratory capacity upon the same stress. Using transmission electron microscopy, we show that fat body and hindgut mitochondria swell, and occasionally burst, upon exposure of the freeze-sensitive phenotype to lethal freezing stress. By contrast, mitochondrial swelling is not observed in the freeze-tolerant phenotype exposed to the same stress. We hypothesize that mitochondrial swelling results from permeability transition of the inner mitochondrial membrane and loss of its barrier function, which causes osmotic influx of cytosolic water into the matrix. We therefore suggest that the phenotypic transition to diapause and cold acclimation could be associated with adaptive changes that include the protection of the inner mitochondrial membrane against permeability transition and subsequent mitochondrial swelling. Accumulation of high concentrations of proline and other cryoprotective substances might be a part of such adaptive changes as we have shown that freezing-induced mitochondrial swelling was abolished by feeding the freeze-sensitive phenotype larvae on a proline-augmented diet.