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Mitochondrial fission

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https://www.readbyqxmd.com/read/27923790/dynamin-related-protein-1-mediates-low-glucose-induced-endothelial-dysfunction-in-human-arterioles
#1
Michael John Tanner, Jingli Wang, Rong Ying, Tisha B Suboc, Mobin Malik, Allison Couillard, Amberly Branum, Venkata Puppala, Michael Eric Widlansky
Intensive glycemic regulation has resulted in an increased incidence of hypoglycemia. Hypoglycemic burden correlates with adverse cardiovascular complications and contributes acutely and chronically to endothelial dysfunction. Prior data indicate mitochondrial dysfunction contributes to hypoglycemia-induced endothelial dysfunction, but the mechanisms behind this linkage remain unknown. We attempt to determine whether clinically relevant low glucose (LG) exposures acutely induce endothelial dysfunction through activation of the mitochondrial fission process...
December 6, 2016: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/27923046/mitochondria-and-caspases-tune-nmnat-mediated-stabilization-to-promote-axon-regeneration
#2
Li Chen, Derek M Nye, Michelle C Stone, Alexis T Weiner, Kyle W Gheres, Xin Xiong, Catherine A Collins, Melissa M Rolls
Axon injury can lead to several cell survival responses including increased stability and axon regeneration. Using an accessible Drosophila model system, we investigated the regulation of injury responses and their relationship. Axon injury stabilizes the rest of the cell, including the entire dendrite arbor. After axon injury we found mitochondrial fission in dendrites was upregulated, and that reducing fission increased stabilization or neuroprotection (NP). Thus axon injury seems to both turn on NP, but also dampen it by activating mitochondrial fission...
December 6, 2016: PLoS Genetics
https://www.readbyqxmd.com/read/27921253/aberrant-alterations-of-mitochondrial-factors-drp1-and-opa1-in-the-brains-of-scrapie-experiment-rodents
#3
Xiao -Dong Yang, Qi Shi, Jing Sun, Yan Lv, Yue Ma, Cao Chen, Kang Xiao, Wei Zhou, Xiao-Ping Dong
The abnormal mitochondrial dynamics has been reported in the brains of some neurodegenerative diseases, such as Alzheimer's disease (AD) and Parkinson's disease (PD), but limitedly described in prion disease. Dynamin-related protein 1 (Drpl) and optic atrophy protein 1 (Opa1) are two essential elements for mitochondria fission and fusion. To evaluate possible changes of mitochondria dynamics during prion infection, the situations of brain Drp1 and Opa1 of scrapie strains 139A, ME7, and S15 mice, as well as 263K-infected hamsters, were analyzed...
December 6, 2016: Journal of Molecular Neuroscience: MN
https://www.readbyqxmd.com/read/27920125/structures-of-human-mitofusin-1-provide-insight-into-mitochondrial-tethering
#4
Yuanbo Qi, Liming Yan, Caiting Yu, Xiangyang Guo, Xin Zhou, Xiaoyu Hu, Xiaofang Huang, Zihe Rao, Zhiyong Lou, Junjie Hu
Mitochondria undergo fusion and fission. The merging of outer mitochondrial membranes requires mitofusin (MFN), a dynamin-like GTPase. How exactly MFN mediates membrane fusion is poorly understood. Here, we determined crystal structures of a minimal GTPase domain (MGD) of human MFN1, including the predicted GTPase and the distal part of the C-terminal tail (CT). The structures revealed that a helix bundle (HB) formed by three helices extending from the GTPase and one extending from the CT closely attaches to the GTPase domain, resembling the configuration of bacterial dynamin-like protein...
December 5, 2016: Journal of Cell Biology
https://www.readbyqxmd.com/read/27913683/mitochondrial-fission-and-fusion
#5
REVIEW
Hakjoo Lee, Yisang Yoon
Mitochondrial fission and fusion have been recognized as critical processes in the health of mitochondria and cells. Two decades of studies have generated a great deal of information about mitochondrial fission and fusion; however, still much needs to be understood for the basic molecular mechanisms of these important cellular processes. The core protein factors for mitochondrial fission and fusion are dynamin proteins that possess membrane-remodeling properties. This short review covers a recent development and understanding of the mechanisms by which these mechanochemical enzymes mediate mitochondrial fission and fusion...
December 15, 2016: Biochemical Society Transactions
https://www.readbyqxmd.com/read/27911875/autophagy-flux-induced-by-ginsenoside-rg3-attenuates-human-prion-protein-mediated-neurotoxicity-and-mitochondrial-dysfunction
#6
Ji-Hong Moon, Ju-Hee Lee, You-Jin Lee, Sang-Youel Park
Mitochondrial quality control is a process by which mitochondria undergo successive rounds of fusion and fission with dynamic exchange of components to segregate functional and damaged elements. Removal of mitochondrion that contains damaged components is accomplished via autophagy. In this study, we investigated whether ginsenoside Rg3, an active ingredient of the herbal medicine ginseng that is used as a tonic and restorative agent, could attenuate prion peptide, PrP (106-126)-induced neurotoxicity and mitochondrial damage...
November 30, 2016: Oncotarget
https://www.readbyqxmd.com/read/27909098/reversible-disruption-of-neuronal-mitochondria-by-ischemic-and-traumatic-injury-revealed-by-quantitative-two-photon-imaging-in-the-neocortex-of-anesthetized-mice
#7
Mikhail Kislin, Jeremy Sword, Ioulia V Fomitcheva, Deborah Croom, Evgeny Pryazhnikov, Eero Lihavainen, Dmytro Toptunov, Heikki Rauvala, Andre S Ribeiro, Leonard Khiroug, Sergei A Kirov
: Mitochondria play a variety of functional roles in cortical neurons, from metabolic support and neuroprotection to the release of cytokines that trigger apoptosis. In dendrites, mitochondrial structure is closely linked to their function, and fragmentation (fission) of the normally elongated mitochondria indicates loss of their function under such pathological conditions as stroke and brain trauma. Using in vivo two-photon microscopy in mouse brain, we quantified mitochondrial fragmentation in a full spectrum of cortical injuries ranging from severe to mild...
December 1, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/27902423/characterization-of-cis-elements-in-the-promoter-of-trz2-encoding-schizosaccharomyces-pombe-mitochondrial-trna-3-end-processing-enzyme
#8
Jinyu Liu, Linting Huang, Yirong Wang, Ying Huang
The endonuclease tRNase Z is responsible for the 3'-end processing of tRNA precursors, which is one of the essential steps in tRNA maturation. The fission yeast Schizosaccharomyces pombe contains two essential tRNase ZL genes (trz1 and trz2) involved in nuclear and mitochondrial tRNA 3'-end processing, respectively. Our previous studies suggest that trz2 is expressed at a very low level. Here we report characterization of the trz2 promoter. Using lacZ as a reporter, we show that the trz2 promoter contains a HomolD box and a very weak diverged TATA element...
November 22, 2016: Microbiology
https://www.readbyqxmd.com/read/27889639/sulforaphane-is-a-nrf2-independent-inhibitor-of-mitochondrial-fission
#9
Gary B O'Mealey, William L Berry, Scott M Plafker
The KEAP1-Nrf2-ARE antioxidant system is a principal means by which cells respond to oxidative and xenobiotic stresses. Sulforaphane (SFN), an electrophilic isothiocyanate derived from cruciferous vegetables, activates the KEAP1-Nrf2-ARE pathway and has become a molecule-of-interest in the treatment of diseases in which chronic oxidative stress plays a major etiological role. We demonstrate here that the mitochondria of cultured, human retinal pigment epithelial (RPE-1) cells treated with SFN undergo hyperfusion that is independent of both Nrf2 and its cytoplasmic inhibitor KEAP1...
November 21, 2016: Redox Biology
https://www.readbyqxmd.com/read/27889468/mitochondrial-cristae-remodelling-is-associated-with-disrupted-opa1-oligomerisation-in-the-huntington-s-disease-r6-2-fragment-model
#10
Tanja Hering, Kerstin Kojer, Nathalie Birth, Jaqueline Hallitsch, Jan-Willem Taanman, Michael Orth
There is evidence of an imbalance of mitochondrial fission and fusion in patients with Huntington's disease (HD) and HD animal models. Fission and fusion are important for mitochondrial homeostasis including mitochondrial DNA (mtDNA) maintenance and may be relevant for the selective striatal mtDNA depletion that we observed in the R6/2 fragment HD mouse model. We aimed to investigate the fission/fusion balance and the integrity of the mitochondrial membrane system in cortex and striatum of end-stage R6/2 mice and wild-type animals...
November 23, 2016: Experimental Neurology
https://www.readbyqxmd.com/read/27889261/nik-map3k14-regulates-mitochondrial-dynamics-and-trafficking-to-promote-cell-invasion
#11
Ji-Ung Jung, Sowndharya Ravi, Dong W Lee, Kassandra McFadden, Michael L Kamradt, L Gerard Toussaint, Raquel Sitcheran
Although the role of NF-κB-inducing kinase (NIK) in immunity is well established, its relevance in cancer is just emerging. Here we describe novel functions for NIK in regulating mitochondrial dynamics and motility to promote cell invasion. We show that NIK is localized to mitochondria in cancer cell lines, ex vivo tumor tissue, and mouse embryonic fibroblasts (MEFs). NIK promotes mitochondrial fission, velocity, and directional migration, resulting in subcellular distribution of mitochondria to the periphery of migrating cells...
November 15, 2016: Current Biology: CB
https://www.readbyqxmd.com/read/27887640/functional-and-regulatory-profiling-of-energy-metabolism-in-fission-yeast
#12
Michal Malecki, Danny A Bitton, Maria Rodríguez-López, Charalampos Rallis, Noelia Garcia Calavia, Graeme C Smith, Jürg Bähler
BACKGROUND: The control of energy metabolism is fundamental for cell growth and function and anomalies in it are implicated in complex diseases and ageing. Metabolism in yeast cells can be manipulated by supplying different carbon sources: yeast grown on glucose rapidly proliferates by fermentation, analogous to tumour cells growing by aerobic glycolysis, whereas on non-fermentable carbon sources metabolism shifts towards respiration. RESULTS: We screened deletion libraries of fission yeast to identify over 200 genes required for respiratory growth...
November 25, 2016: Genome Biology
https://www.readbyqxmd.com/read/27884323/the-toll-like-receptor-4-antagonist-transforming-growth-factor-%C3%AE-activated-kinase-tak-242-attenuates-taurocholate-induced-oxidative-stress-through-regulating-mitochondrial-function-in-mice-pancreatic-acinar-cells
#13
Long-Fei Pan, Lei Yu, Li-Ming Wang, Jun-Tao He, Jiang-Li Sun, Xiao-Bo Wang, Zheng-Hai Bai, Li-Juan Su, Hong-Hong Pei
BACKGROUND: Acute pancreatitis (AP) is a commonly occurring and potentially life-threatening disease. Recently, toll-like receptor 4 (TLR4) has been considered as a new clue for studying the pathogenesis of AP due to its important role in inflammatory response cascade. MATERIALS AND METHODS: The aim of this study was to investigate the potential protective effect of transforming growth factor-β-activated kinase (TAK)-242, a novel TLR4 antagonist, in taurocholate-treated mice pancreatic acinar cells...
December 2016: Journal of Surgical Research
https://www.readbyqxmd.com/read/27876411/disruption-of-mitochondrial-quality-control-in-peripheral-artery-disease-new-therapeutic-opportunities
#14
REVIEW
Cintia B Ueta, Katia S Gomes, Márcio A Ribeiro, Daria Mochly-Rosen, Julio C B Ferreira
Peripheral artery disease (PAD) is a multifactorial disease initially triggered by reduced blood supply to the lower extremities due to atherosclerotic obstructions. It is considered a major public health problem worldwide, affecting over 200 million people. Management of PAD includes smoking cessation, exercise, statin therapy, antiplatelet therapy, antihypertensive therapy and surgical intervention. Although these pharmacological and non-pharmacological interventions usually increases blood flow to the ischemic limb, morbidity and mortality associated with PAD continue to increase...
November 19, 2016: Pharmacological Research: the Official Journal of the Italian Pharmacological Society
https://www.readbyqxmd.com/read/27875077/march5-rna-promotes-autophagy-migration-and-invasion-of-ovarian-cancer-cells
#15
Jianguo Hu, Ying Meng, Zhanqin Zhang, Qiuting Yan, Xingwei Jiang, Zilan Lv, Lina Hu
MARCH5 is a crucial regulator of mitochondrial fission. However, the expression and function of MARCH5 in ovarian cancer have not been determined. This study investigated the expression and function of MARCH5 in ovarian cancer with respect to its potential role in the tumorigenesis of the disease as well as its usefulness as an early diagnostic marker. We found that the expression of MARCH5 was substantially upregulated in ovarian cancer tissue in comparison with the normal control. Silencing MARCH5 in SKOV3 cells decreased TGFB1-induced cell macroautophagy/autophagy, migration, and invasion in vitro and in vivo, whereas the ectopic expression of MARCH5 in A2780 cells had the opposite effect...
November 22, 2016: Autophagy
https://www.readbyqxmd.com/read/27869201/cardioprotection-by-combination-of-three-compounds-from-shengmai-preparations-in-mice-with-myocardial-ischemia-reperfusion-injury-through-ampk-activation-mediated-mitochondrial-fission
#16
Fang Li, Xiaoxue Fan, Yu Zhang, Lizhi Pang, Xiaonan Ma, Meijia Song, Junping Kou, Boyang Yu
GRS is a drug combination of three active components including ginsenoside Rb1, ruscogenin and schisandrin. It derived from the well-known TCM formula ShengMai preparations, a widely used traditional Chinese medicine for the treatment of cardiovascular diseases in clinic. The present study explores the cardioprotective effects of GRS on myocardial ischemia/reperfusion (MI/R) injury compared with ShengMai preparations and investigates the underlying mechanisms. GRS treatment significantly attenuated MI/R injury and exhibited similar efficacy as Shengmai preparations, as evidenced by decreased myocardium infarct size, ameliorated histological features, the decrease of LDH production and improved cardiac function, and also produced a significant decrease of apoptotic index...
November 21, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27863209/mouse-tmem135-mutation-reveals-a-mechanism-involving-mitochondrial-dynamics-that-leads-to-age-dependent-retinal-pathologies
#17
Wei-Hua Lee, Hitoshi Higuchi, Sakae Ikeda, Erica L Macke, Tetsuya Takimoto, Bikash R Pattnaik, Che Liu, Li-Fang Chu, Sandra M Siepka, Kathleen J Krentz, C Dustin Rubinstein, Robert F Kalejta, James A Thomson, Robert F Mullins, Joseph S Takahashi, Lawrence H Pinto, Akihiro Ikeda
While the aging process is central to the pathogenesis of age-dependent diseases, it is poorly understood at the molecular level. We identified a mouse mutant with accelerated aging in the retina as well as pathologies observed in age-dependent retinal diseases, suggesting that the responsible gene regulates retinal aging, and its impairment results in age-dependent disease. We determined that a mutation in the transmembrane 135 (Tmem135) is responsible for these phenotypes. We observed localization of TMEM135 on mitochondria, and imbalance of mitochondrial fission and fusion in mutant Tmem135 as well as Tmem135 overexpressing cells, indicating that TMEM135 is involved in the regulation of mitochondrial dynamics...
November 15, 2016: ELife
https://www.readbyqxmd.com/read/27862231/early-stage-functions-of-mitochondrial-autophagy-and-oxidative-stress-in-acetaminophen-induced-liver-injury
#18
Yan Gao, Shifeng Chu, Zhao Zhang, Wei Zuo, Congyuan Xia, Qidi Ai, Piao Luo, Peng Cao, Naihong Chen
Mitochondria go through frequent cycles of fusion and fission, a process required for mitochondrial quality control by eliminating ROS-damaged mitochondria through mitochondrial autophagy. Acetaminophen (APAP) overdose can cause liver injury in animals and human beings by inducing mitochondrial damage, which need to be further evaluated. The aim of the current study is to assess the changes between oxidative damage and mitophagy in vivo and in vitro, which mimics APAP-induced liver injury (AILI) in humans. Liver damage was monitored by measuring the levels of biochemical indexes...
November 9, 2016: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/27861739/afzelin-ameliorates-d-galactosamine-and-lipopolysaccharide-induced-fulminant-hepatic-failure-by-modulating-mitochondrial-quality-control-and-dynamics-150-150
#19
Sang-Bin Lee, Jung-Woo Kang, So-Jin Kim, Jongmin Ahn, Jinwoong Kim, Sun-Mee Lee
BACKGROUND AND PURPOSE: Fulminant hepatic failure (FHF) is a fatal clinical syndrome that results in excessive inflammation and hepatocyte death. Mitochondrial dysfunction is considered to be a possible mechanism of FHF. Afzelin, a flavonol glycoside found in Houttuynia cordata Thunberg, has anti-inflammatory and antioxidant properties. The present study elucidated the cytoprotective mechanisms of afzelin against D-galactosamine (GalN)/lipopolysaccharide (LPS)-induced FHF, particularly focusing on mitochondrial quality control and dynamics...
November 15, 2016: British Journal of Pharmacology
https://www.readbyqxmd.com/read/27858084/a-threshold-of-transmembrane-potential-is-required-for-mitochondrial-dynamic-balance-mediated-by-drp1-and-oma1
#20
Edith Jones, Norma Gaytan, Iraselia Garcia, Alan Herrera, Manuel Ramos, Divya Agarwala, Maahrose Rana, Wendy Innis-Whitehouse, Erin Schuenzel, Robert Gilkerson
As an organellar network, mitochondria dynamically regulate their organization via opposing fusion and fission pathways to maintain bioenergetic homeostasis and contribute to key cellular pathways. This dynamic balance is directly linked to bioenergetic function: loss of transmembrane potential across the inner membrane (Δψ m) disrupts mitochondrial fission/fusion balance, causing fragmentation of the network. However, the level of Δψ m required for mitochondrial dynamic balance, as well as the relative contributions of fission and fusion pathways, have remained unclear...
November 17, 2016: Cellular and Molecular Life Sciences: CMLS
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