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https://www.readbyqxmd.com/read/29324904/prohibitin-plays-a-critical-role-in-enterovirus-71-neuropathogenesis
#1
Issac Horng Khit Too, Isabelle Bonne, Eng Lee Tan, Justin Jang Hann Chu, Sylvie Alonso
A close relative of poliovirus, enterovirus 71 (EV71) is regarded as an important neurotropic virus of serious public health concern. EV71 causes Hand, Foot and Mouth Disease and has been associated with neurological complications in young children. Our limited understanding of the mechanisms involved in its neuropathogenesis has hampered the development of effective therapeutic options. Here, using a two-dimensional proteomics approach combined with mass spectrometry, we have identified a unique panel of host proteins that were differentially and dynamically modulated during EV71 infection of motor-neuron NSC-34 cells, which are found at the neuromuscular junctions where EV71 is believed to enter the central nervous system...
January 2018: PLoS Pathogens
https://www.readbyqxmd.com/read/29323705/the-protective-effects-of-distal-ischemic-treatment-on-apoptosis-and-mitochondrial-permeability-in-the-hippocampus-after-cardiopulmonary-resuscitation
#2
Xiang Zhou, Liu Yong, Yang Huang, ShuiBo Zhu, XiaoYang Song, BiXi Li, Jian Zhu, HaiBo Wang
BACKGROUND: Apoptosis and mitochondrial dysfunction are the main cause of neurological injury after cardiopulmonary resuscitation (CPR). However, the effects of distal ischemic treatments on ischemia-induced apoptosis are rarely studied, and the mechanism by which mitochondrial dysfunction contributes to CPR still unclear. METHODS: A rat model of distal ischemia was established by clipping the right femoral artery. Rats were divided into blank, model, pre-distal ischemic treatment, per-treatment, and post-treatment groups...
January 11, 2018: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/29318513/targeted-elimination-of-mutant-mitochondrial-dna-in-melas-ipscs-by-mitotalens
#3
Yi Yang, Han Wu, Xiangjin Kang, Yanhui Liang, Ting Lan, Tianjie Li, Tao Tan, Jiangyun Peng, Quanjun Zhang, Geng An, Yali Liu, Qian Yu, Zhenglai Ma, Ying Lian, Boon Seng Soh, Qingfeng Chen, Ping Liu, Yaoyong Chen, Xiaofang Sun, Rong Li, Xiumei Zhen, Ping Liu, Yang Yu, Xiaoping Li, Yong Fan
Mitochondrial diseases are maternally inherited heterogeneous disorders that are primarily caused by mitochondrial DNA (mtDNA) mutations. Depending on the ratio of mutant to wild-type mtDNA, known as heteroplasmy, mitochondrial defects can result in a wide spectrum of clinical manifestations. Mitochondria-targeted endonucleases provide an alternative avenue for treating mitochondrial disorders via targeted destruction of the mutant mtDNA and induction of heteroplasmic shifting. Here, we generated mitochondrial disease patient-specific induced pluripotent stem cells (MiPSCs) that harbored a high proportion of m...
January 9, 2018: Protein & Cell
https://www.readbyqxmd.com/read/29317574/-role-of-immune-related-gtpase-m1-in-cortical-neurons-autophagy-of-mice-with-sepsis-induced-brain-injury
#4
Qun Huang, Bin Chen, Yafei Li, Xihong Li
To investigate the role of immune-related GTPase M1 (IRGM1) in cortical neurons autophagy in mice with sepsis induced brain injury (SIBI).
 Methods: Sixty wild-type C57BL/6 mice and sixty IRGM1 gene knockout C57BL/6 mice were randomly divided into 4 groups: a sham-operated wild-type (SWT) group, a cecal ligation and puncture (CLP) model wild-type (MWT) group, a sham-operated knockout (SKO) group, and a CLP model knockout (MKO) group. Models of mice with sepsis were established by CLP. Six hours of after CLP, the neurobehavioral scores for mice were recorded...
December 28, 2017: Zhong Nan da Xue Xue Bao. Yi Xue Ban, Journal of Central South University. Medical Sciences
https://www.readbyqxmd.com/read/29317196/protonophoric-action-of-triclosan-causes-calcium-efflux-from-mitochondria-plasma-membrane-depolarization-and-bursts-of-miniature-end-plate-potentials
#5
Lyudmila B Popova, Ekaterina S Nosikova, Elena A Kotova, Ekaterina O Tarasova, Pavel A Nazarov, Lyudmila S Khailova, Olga P Balezina, Yuri N Antonenko
The formerly widely used broad-spectrum biocide triclosan (TCS) has now become a subject of special concern due to its accumulation in the environment and emerging diverse toxicity. Despite the common opinion that TCS is an uncoupler of oxidative phosphorylation in mitochondria, there have been so far no studies of protonophoric activity of this biocide on artificial bilayer lipid membranes (BLM). Yet only few works have indicated the relationship between TCS impacts on mitochondria and nerve cell functioning...
January 6, 2018: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/29316798/regulation-of-mitophagy-by-the-ubiquitin-pathway-in-neurodegenerative-diseases
#6
Shyamal Desai, Meredith Juncker, Catherine Kim
Mitophagy is a cellular process by which dysfunctional mitochondria are degraded via autophagy. Increasing empirical evidence proposes that this mitochondrial quality-control mechanism is defective in neurons of patients with various neurodegenerative diseases such as Ataxia Telangiectasia, Alzheimer's disease, Parkinson's disease, and Amyotrophic Lateral Sclerosis. Accumulation of defective mitochondria and the production of reactive oxygen species due to defective mitophagy have been identified as causes underlying neurodegenerative disease pathogenesis...
January 1, 2018: Experimental Biology and Medicine
https://www.readbyqxmd.com/read/29315581/parkinson-disease-related-dj-1-modulates-the-expression-of-uncoupling-protein-4-against-oxidative-stress
#7
Shaoqing Xu, Xiaodong Yang, Yiwei Qian, Qin Xiao
Loss of function mutations of DJ-1 (PARK7) have been linked to the pathogenesis of Parkinson disease (PD). Antioxidative stress is one of the multi-protective functions of DJ-1, and oxidation of cysteine 106 (Cys106) has been proposed to regulate the protective activity of DJ-1. Uncoupling protein 4 (UCP4) is located in the inner membrane of mitochondria and functions to protect against oxidative stress. In this study, we used neuronal (SH-SY5Y) cells and DJ-1 knockout (KO) mice to elucidate whether DJ-1 regulated oxidative stress via modulating the expression of UCP4, and the underlying mechanism...
January 8, 2018: Journal of Neurochemistry
https://www.readbyqxmd.com/read/29314450/ellagic-acid-mitigates-arsenic-trioxide-induced-mitochondrial-dysfunction-and-cytotoxicity-in-sh-sy5y-cells
#8
Fakiha Firdaus, Mohd Faraz Zafeer, Mohammad Waseem, Ehraz Anis, M Mobarak Hossain, Mohammad Afzal
In the current study, neuroprotective significance of ellagic acid (EA, a polyohenol) was explored by primarily studying its antioxidant and antiapoptotic potential against arsenic trioxide (As2 O3 )-induced toxicity in SH-SY5Y human neuroblastoma cell lines. The mitigatory effects of EA with particular reference to cell viability and cytotoxicity, the generation of reactive oxygen species, DNA damage, and mitochondrial dynamics were studied. Pretreatment of SH-SY5Y cells with EA (10 and 20 μM) for 60 min followed by exposure to 2 μM As2 O3 protected the SH-SY5Y cells against the harmful effects of the second...
January 4, 2018: Journal of Biochemical and Molecular Toxicology
https://www.readbyqxmd.com/read/29311649/high-content-image-analysis-reveals-function-of-mir-124-upstream-of-vimentin-in-regulating-motor-neuron-mitochondria
#9
Tal Yardeni, Raquel Fine, Yuvraj Joshi, Tal Gradus-Pery, Noga Kozer, Irit Reichenstein, Eran Yanowski, Shir Nevo, Hila Weiss-Tishler, Michal Eisenberg-Bord, Tal Shalit, Alexander Plotnikov, Haim M Barr, Eran Perlson, Eran Hornstein
microRNAs (miRNAs) are critical for neuronal function and their dysregulation is repeatedly observed in neurodegenerative diseases. Here, we implemented high content image analysis for investigating the impact of several miRNAs in mouse primary motor neurons. This survey directed our attention to the neuron-specific miR-124, which controls axonal morphology. By performing next generation sequencing analysis and molecular studies, we characterized novel roles for miR-124 in control of mitochondria localization and function...
January 8, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29310663/%C3%AE-synuclein-accumulation-and-gba-deficiency-due-to-l444p-gba-mutation-contributes-to-mptp-induced-parkinsonism
#10
Seung Pil Yun, Donghoon Kim, Sangjune Kim, SangMin Kim, Senthilkumar S Karuppagounder, Seung-Hwan Kwon, Saebom Lee, Tae-In Kam, Suhyun Lee, Sangwoo Ham, Jae Hong Park, Valina L Dawson, Ted M Dawson, Yunjong Lee, Han Seok Ko
BACKGROUND: Mutations in glucocerebrosidase (GBA) cause Gaucher disease (GD) and increase the risk of developing Parkinson's disease (PD) and Dementia with Lewy Bodies (DLB). Since both genetic and environmental factors contribute to the pathogenesis of sporadic PD, we investigated the susceptibility of nigrostriatal dopamine (DA) neurons in L444P GBA heterozygous knock-in (GBA +/L444P ) mice to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a selective dopaminergic mitochondrial neurotoxin...
January 8, 2018: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/29303602/melatonin-attenuates-chronic-cough-mediated-by-oxidative-stress-via-transient-receptor-potential-melastatin-2-in-guinea-pigs-exposed-to-particulate-matter-2-5
#11
Zhenjun Ji, Zhen Wang, Zhe Chen, Hao Jin, Chen Chen, Senlin Chai, Haining Lv, Ling Yang, Yakun Hu, Rong Dong, Kefang Lai
The aim of this study was to investigate the effects of melatonin on oxidative stress, the expression of transient receptor potential melastatin-2 (TRPM2) in guinea pig brains, and the influence of melatonin on oxidative stress in lungs and airway inflammation induced by particulate matter 2.5 (PM2.5). A particle suspension (0.1 g/ml) was nasally administered to the guinea pigs to prepare a PM2.5 exposure model. Cough frequency and cough incubation period were determined through RM6240B biological signal collection and disposal system...
January 5, 2018: Physiological Research
https://www.readbyqxmd.com/read/29295823/the-stress-induced-transcription-factor-nr4a1-adjusts-mitochondrial-function-and-synapse-number-in-prefrontal-cortex
#12
Freddy Jeanneteau, Christian Barrère, Mariska Vos, Carlie Jm De Vries, Claude Rouillard, Daniel Levesque, Yann Dromard, Marie-Pierre Moisan, Vanja Duric, Tina C Franklin, Ronald S Duman, David A Lewis, Stephen D Ginsberg, Margarita Arango-Lievano
The energetic costs of behavioral chronic stress are unlikely to be sustainable without neuronal plasticity. Mitochondria have the capacity to handle synaptic activity up to a limit before energetic depletion occurs. Protective mechanisms driven by the induction of neuronal genes likely evolved to buffer the consequences of chronic stress on excitatory neurons in prefrontal cortex (PFC), as this circuitry is vulnerable to excitotoxic insults. Little is known about the genes involved in mitochondrial adaptation to the build up of chronic stress...
January 2, 2018: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/29290944/mitochondrial-targeted-hsp90-inhibitor-gamitrinib-tpp-g-tpp-induces-pink1-parkin-dependent-mitophagy
#13
Fabienne C Fiesel, Elle D James, Roman Hudec, Wolfdieter Springer
Loss-of-function mutations in PINK1 or PARKIN are associated with early-onset Parkinson's disease. Upon mitochondrial stress, PINK1 and Parkin together mediate a response that protects cells from the accumulation of harmful, damaged mitochondria. PINK1, the upstream kinase accumulates on the mitochondrial surface and recruits the E3 ubiquitin ligase Parkin on site to ubiquitylate substrate proteins. The joint activity of both to generate phosphorylated poly-ubiquitin chains on the mitochondrial surface induces the recruitment of autophagy receptors and eventually whole organelles are cleared by autophagy...
December 5, 2017: Oncotarget
https://www.readbyqxmd.com/read/29289695/calpain-and-jnk-pathways-participate-in-isoflurane-induced-nucleus-translocation-of-apoptosis-inducing-factor-in-the-brain-of-neonatal-rats
#14
Xue Han, Chuiliang Liu, Kun Zhang, Mingyan Guo, Zhiwen Shen, Yafang Liu, Zhiyi ZuoDeg, Minghui Cao, Yujuan Li
Recent studies have demonstrated that volatile anesthetic causes caspase-dependent neuroapoptosis and persistent cognitive deficits in young animals. Apoptosis-inducing factor (AIF) can trigger apoptosis by caspase-independent pathway. Whether isoflurane induces neuroapoptosis by activation of AIF and its possible mechanism are underdetermined. Rats at postnatal day 7 were exposed to 1.1% isoflurane for 4 h and the expression of AIF, cytochrome c, caspase-3, μ-calpain, m-calpain, Bcl-2 and Bax in the mitochondrial, cytosolic, and nuclear fraction, as well as the number of both AIF and TUNEL positive neurons in the cortices of rats were measured...
December 28, 2017: Toxicology Letters
https://www.readbyqxmd.com/read/29289598/why-should-neuroscientists-worry-about-iron-the-emerging-role-of-ferroptosis-in-the-pathophysiology-of-neuroprogressive-diseases
#15
REVIEW
Gerwyn Morris, Michael Berk, André F Carvalho, Michael Maes, Adam J Walker, Basant K Puri
Ferroptosis is a unique form of programmed death, characterised by cytosolic accumulation of iron, lipid hydroperoxides and their metabolites, and effected by the fatal peroxidation of polyunsaturated fatty acids in the plasma membrane. It is a major driver of cell death in neurodegenerative neurological diseases. Moreover, cascades underpinning ferroptosis could be active drivers of neuropathology in major psychiatric disorders. Oxidative and nitrosative stress can adversely affect mechanisms and proteins governing cellular iron homeostasis, such as the iron regulatory protein/iron response element system, and can ultimately be a source of abnormally high levels of iron and a source of lethal levels of lipid membrane peroxidation...
December 28, 2017: Behavioural Brain Research
https://www.readbyqxmd.com/read/29288688/neuroprotective-activity-of-macamides-on-manganese-induced-mitochondrial-disruption-in-u-87-mg-glioblastoma-cells
#16
Kuljeet S Gugnani, Nguyen Vu, Alejandro N Rondón-Ortiz, Mark Böhlke, Timothy J Maher, Alejandro J Pino-Figueroa
Macamides are a distinct class of secondary metabolites, benzylamides of long chain fatty acids, which were isolated from the Peruvian plant Lepidium meyenii (Maca). As structural analogues of the endocannabinoid anandamide (AEA), they have demonstrated neuroprotective effects in vitro and in vivo. The purpose of this study was to demonstrate the neuroprotective activity of the macamides: N-(3-methoxybenzyl)oleamide (MAC 18:1), N-(3-methoxybenzyl)linoleamide (MAC 18:2) and N-(3-methoxybenzyl)linolenamide (MAC 18:3) in a neurotoxic environment caused by exposure of U-87 MG glioblastoma cells to manganese chloride (MnCl2)...
December 27, 2017: Toxicology and Applied Pharmacology
https://www.readbyqxmd.com/read/29283047/is-it-all-said-for-nsaids-in-alzheimer-s-disease-role-of-mitochondrial-calcium-uptake
#17
Sara Sanz-Blasco, Maria Calvo-Rodríguez, Erica Caballero, Monica Garcia-Durillo, Lucía Nunez, Carlos Villalobos
Epidemiological data suggest that non-steroidal anti-inflammatory drugs (NSAIDs) may protect against Alzheimer's disease (AD). Unfortunately, recent trials have failed in providing compelling evidence of neuroprotection. Discussion as to why NSAIDs effectivity is uncertain is ongoing. Possible explanations include the view that NSAIDs and other possible disease-modifying drugs should be provided before the patients develop symptoms of AD or cognitive decline. In addition, NSAID targets for neuroprotection are unclear...
December 27, 2017: Current Alzheimer Research
https://www.readbyqxmd.com/read/29282769/glial-m6b-stabilizes-the-axonal-membrane-at-peripheral-nodes-of-ranvier
#18
Marie L Bang, Anya Vainshtein, Hyun-Jeong Yang, Yael Eshed-Eisenbach, Jerome Devaux, Hauke B Werner, Elior Peles
Glycoprotein M6B and the closely related proteolipid protein regulate oligodendrocyte myelination in the central nervous system, but their role in the peripheral nervous system is less clear. Here we report that M6B is located at nodes of Ranvier in peripheral nerves where it stabilizes the nodal axolemma. We show that M6B is co-localized and associates with gliomedin at Schwann cell microvilli that are attached to the nodes. Developmental analysis of sciatic nerves, as well as of myelinating Schwann cells/dorsal root ganglion neurons cultures, revealed that M6B is already present at heminodes, which are considered the precursors of mature nodes of Ranvier...
December 28, 2017: Glia
https://www.readbyqxmd.com/read/29281123/mitochondrial-dna-damage-and-reactive-oxygen-species-in-neurodegenerative-disease
#19
REVIEW
Nadee Nissanka, Carlos T Moraes
Mitochondria are essential organelles within the cell where most ATP is produced through oxidative phosphorylation (OXPHOS). A subset of the genes needed for this process are encoded by the mitochondrial DNA (mtDNA). One consequence of OXPHOS is the production of mitochondrial reactive oxygen species (ROS), whose role in mediating cellular damage, particularly in damaging mtDNA during aging, has been controversial. There are subsets of neurons that appear to be more sensitive to ROS-induced damage, and mitochondrial dysfunction has been associated with several neurodegenerative disorders...
December 27, 2017: FEBS Letters
https://www.readbyqxmd.com/read/29277914/synaptic-localization-of-the-sumoylation-regulating-protease-senp5-in-the-adult-mouse-brain
#20
Hiroki Akiyama, Kazuhiko Nakadate, Shin-Ichi Sakakibara
Covalent conjugation of small ubiquitin-like modifiers (SUMOs) or SUMOylation is a reversible post-translational modification that regulates the stability and function of target proteins. SUMOs are removed from substrate proteins by sentrin/SUMO-specific proteases (SENPs). Numerous studies have implicated SUMOylation in various physiological and pathological processes in neurons. To understand the functional roles of SUMOylation, it is necessary to determine the distribution of enzymes regulating SUMO conjugation and deconjugation; yet, the localization of SENPs has not been described in detail in intact brain tissue...
December 26, 2017: Journal of Comparative Neurology
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