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https://www.readbyqxmd.com/read/29656361/characterization-of-the-mitochondrial-aerobic-metabolism-in-the-pre-and-perisynaptic-districts-of-the-sod1-g93a-mouse-model-of-amyotrophic-lateral-sclerosis
#1
Silvia Ravera, Tiziana Bonifacino, Martina Bartolucci, Marco Milanese, Elena Gallia, Francesca Provenzano, Katia Cortese, Isabella Panfoli, Giambattista Bonanno
Amyotrophic lateral sclerosis (ALS) is an adult-onset fatal neurodegenerative disease characterized by muscle wasting, weakness, and spasticity due to a progressive degeneration of cortical, brainstem, and spinal motor neurons. The etiopathological causes are still largely obscure, although astrocytes definitely play a role in neuronal damage. Several mechanisms have been proposed to concur to neurodegeneration in ALS, including mitochondrial dysfunction. We have previously shown profound modifications of glutamate release and presynaptic plasticity in the spinal cord of the SOD1 G93A mouse model of ALS...
April 14, 2018: Molecular Neurobiology
https://www.readbyqxmd.com/read/29653138/neuroprotective-action-of-4-hydroxyisophthalic-acid-against-paraquat-induced-motor-impairment-involves-amelioration-of-mitochondrial-damage-and-neurodegeneration-in-drosophila
#2
Niveditha S, T Shivanandappa
Neurodegenerative disorders including Parkinson's disease (PD) are believed to be caused by oxidative stress and mitochondrial dysfunction. Exposure to environmental agents such as pesticides has been implicated in the etiology of sporadic PD. Paraquat (PQ), a widely used herbicide, induces PD symptoms in laboratory animals including Drosophila. PQ acts as a free radical generator and induces oxidative damage, which is implicated in neuronal cell death. Drosophila model of PQ-induced PD offers a convenient tool for mechanistic studies and, to assess the neuroprotective potential of natural antioxidants...
April 10, 2018: Neurotoxicology
https://www.readbyqxmd.com/read/29644580/on-the-efficacy-of-cardio-pulmonary-resuscitation-and-epinephrine-following-cyanide-and-h-2-s-intoxication-induced-cardiac-asystole
#3
Annick Judenherc-HaouzI, Takashi Sonobe, Vikhyat S Bebarta, Philippe Haouzi
This study was aimed at determining the efficacy of epinephrine, followed by chest compressions, in producing a return of spontaneous circulation (ROSC) during cyanide (CN)- or hydrogen sulfide (H2 S)-induced toxic cardiac pulseless electrical activity (PEA) in the rat. Thirty-nine anesthetized rats were exposed to either intravenous KCN (n = 27) or H2 S solutions (n = 12), at a rate that led to a PEA within less than 10 min. In the group intoxicated by CN, 20 rats were mechanically ventilated and received either epinephrine (0...
April 11, 2018: Cardiovascular Toxicology
https://www.readbyqxmd.com/read/29644532/methamphetamine-induces-apoptosis-of-microglia-via-the-intrinsic-mitochondrial-dependent-pathway
#4
Anna V Sharikova, Elizabeth Quaye, Jun Yong Park, Maxwell C Maloney, Habben Desta, Ramkumar Thiyagarajan, Kenneth L Seldeen, Neil U Parikh, Parteet Sandhu, Alexander Khmaladze, Bruce R Troen, Stanley A Schwartz, Supriya D Mahajan
Methamphetamine (METH) is a drug of abuse, the acute and chronic use of which induces neurotoxic responses in the human brain, ultimately leading to neurocognitive disorders. Our goals were to understand the impact of METH on microglial mitochondrial respiration and to determine whether METH induces the activation of the mitochondrial-dependent intrinsic apoptosis pathway in microglia. We assessed the expression of pro- apoptosis genes using qPCR of RNA extracted from a human microglial cell line (HTHU). We examined the apoptosis-inducing effects of METH on microglial cells using digital holographic microscopy (DHM) to quantify real-time apoptotic volume decrease (AVD) in microglia in a noninvasive manner...
April 11, 2018: Journal of Neuroimmune Pharmacology: the Official Journal of the Society on NeuroImmune Pharmacology
https://www.readbyqxmd.com/read/29643477/accurate-estimation-of-5-methylcytosine-in-mammalian-mitochondrial-dna
#5
Shigeru Matsuda, Takehiro Yasukawa, Yuriko Sakaguchi, Kenji Ichiyanagi, Motoko Unoki, Kazuhito Gotoh, Kei Fukuda, Hiroyuki Sasaki, Tsutomu Suzuki, Dongchon Kang
Whilst 5-methylcytosine (5mC) is a major epigenetic mark in the nuclear DNA in mammals, whether or not mitochondrial DNA (mtDNA) receives 5mC modification remains controversial. Herein, we exhaustively analysed mouse mtDNA using three methods that are based upon different principles for detecting 5mC. Next-generation bisulfite sequencing did not give any significant signatures of methylation in mtDNAs of liver, brain and embryonic stem cells (ESCs). Also, treatment with methylated cytosine-sensitive endonuclease McrBC resulted in no substantial decrease of mtDNA band intensities in Southern hybridisation...
April 11, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29643256/critical-role-of-flavin-and-glutathione-in-complex-i-mediated-bioenergetic-failure-in-brain-ischemia-reperfusion-injury
#6
Anja Kahl, Anna Stepanova, Csaba Konrad, Corey Anderson, Giovanni Manfredi, Ping Zhou, Costantino Iadecola, Alexander Galkin
BACKGROUND AND PURPOSE: Ischemic brain injury is characterized by 2 temporally distinct but interrelated phases: ischemia (primary energy failure) and reperfusion (secondary energy failure). Loss of cerebral blood flow leads to decreased oxygen levels and energy crisis in the ischemic area, initiating a sequence of pathophysiological events that after reoxygenation lead to ischemia/reperfusion (I/R) brain damage. Mitochondrial impairment and oxidative stress are known to be early events in I/R injury...
April 11, 2018: Stroke; a Journal of Cerebral Circulation
https://www.readbyqxmd.com/read/29629602/deactivation-of-mitochondrial-complex-i-after-hypoxia-ischemia-in-the-immature-brain
#7
Anna Stepanova, Csaba Konrad, Sergio Guerrero-Castillo, Giovanni Manfredi, Susan Vannucci, Susanne Arnold, Alexander Galkin
Mortality from perinatal hypoxic-ischemic (HI) brain injury reached 1.15 million worldwide in 2010 and is also a major factor for neurological disability in infants. HI directly influences the oxidative phosphorylation enzyme complexes in mitochondria, but the exact mechanism of HI-reoxygenation response in brain remains largely unresolved. After induction of HI-reoxygenation in postnatal day 10 rats, activities of mitochondrial respiratory chain enzymes were analysed and complexome profiling was performed...
January 1, 2018: Journal of Cerebral Blood Flow and Metabolism
https://www.readbyqxmd.com/read/29627876/naringin-attenuates-cerebral-ischemia-reperfusion-injury-through-inhibiting-peroxynitrite-mediated-mitophagy-activation
#8
Jinghan Feng, Xingmiao Chen, Shengwen Lu, Wenting Li, Dan Yang, Weiwei Su, Xijun Wang, Jiangang Shen
Excessive autophagy/mitophagy plays important roles during cerebral ischemia-reperfusion (I/R) injury. Peroxynitrite (ONOO- ), a representative reactive nitrogen species, mediates excessive mitophagy activation and exacerbates cerebral I/R injury. In the present study, we tested the hypothesis that naringin, a natural antioxidant, could inhibit ONOO- -mediated mitophagy activation and attenuate cerebral I/R injury. Firstly, we demonstrated that naringin possessed strong ONOO- scavenging capability and also inhibited the production of superoxide and nitric oxide in SH-SY5Y cells exposed to 10 h oxygen-glucose-deprivation plus 14 h of reoxygenation or ONOO- donor 3-morpholinosydnonimine conditions...
April 7, 2018: Molecular Neurobiology
https://www.readbyqxmd.com/read/29627393/highly-efficient-production-of-functional-recombinant-human-fibroblast-growth-factor-22-in-e-coli-and-its-protective-effects-on-h-2-o-2-lesioned-l02-cells
#9
Huanhuan Yang, Haishan Tian, Jiliang Cheng, Jie Zheng, Dezhong Wang, Changye Sun, David Fernig, Taotao Chen, Weiyue Gong, Shen Wang, Xiaokun Li, Chao Jiang
In the 22 member mammalian FGF family, FGF22 belongs to FGF7 subfamily, and its effects are largely confined to the brain and skin. To explore the functions of FGF22 on other tissues and develop a large-scale production of recombinant human FGF22 (rhFGF22) without a fusion tag, a plasmid encoding human FGF22 (pET3a-rhFGF22) was used to express rhFGF22 in E. coli BL21 (DE3) pLysS. A large amount of rhFGF22 inclusion body protein was obtained. A two-step denaturing method successfully solubilized rhFGF22, and it was refolded and then purified in one step via heparin affinity chromatography...
April 5, 2018: Protein Expression and Purification
https://www.readbyqxmd.com/read/29626647/multiple-pathways-for-mitophagy-a-neurodegenerative-conundrum-for-parkinson-s-disease
#10
REVIEW
Charleen T Chu
It has been nearly a decade since the first landmark studies implicating familial recessive Parkinson's disease genes in the regulation of selective mitochondrial autophagy. The PTEN-induced kinase 1 (PINK1) and the E3 ubiquitin ligase Parkin (encoded by the PARK2 gene) act together to mark depolarized mitochondria for degradation. There is now an extensive body of literature detailing key mediators and steps in this pathway, based mostly on work in transformed cell lines. However, the degree to which PINK1-triggered mitophagy contributes to mitochondrial quality control in the mammalian brain, and the extent to which its disruption contributes to Parkinson's disease pathogenesis remain uncertain...
April 4, 2018: Neuroscience Letters
https://www.readbyqxmd.com/read/29626315/new-views-and-possibilities-of-antidiabetic-drugs-in-treating-and-or-preventing-mild-cognitive-impairment-and-alzheimer-s-disease
#11
REVIEW
Kai Long Zhong, Fang Chen, Hao Hong, Xuan Ke, Yang Ge Lv, Su Su Tang, Yu Bing Zhu
Mounting evidence suggests that diabetes mellitus (DM) is associated with mild cognitive impairment (MCI), vascular dementia and Alzheimer's disease (AD). Biological, clinical and epidemiological data support a close link between DM and AD. Increasingly, studies have found that several antidiabetic agents can promote neurogenesis, and clinically ameliorate cognitive and memory impairments in different clinical settings. Data has shown that these antidiabetic drugs positively affect mitochondrial and synaptic function, neuroinflammation, and brain metabolism...
April 6, 2018: Metabolic Brain Disease
https://www.readbyqxmd.com/read/29625493/characterization-of-a-spontaneously-immortalized-murine-m%C3%A3-ller-glial-cell-line-qmmuc-1
#12
Josy Augustine, Sofia Pavlou, Michael O'Hare, Kevin Harkin, Alan Stitt, Tim Curtis, Heping Xu, Mei Chen
Purpose: Müller glia are critical for the survival of retinal neurons and the integrity of retinal blood vessels. Müller glial cultures are important tools for investigating Müller glial pathophysiology. Here, we report a spontaneously immortalized Müller glial cell line originally cultured and subsequently cloned from mouse pups. The cell line, Queen's University Murine Müller glia Clone-1 (QMMuC-1), has been cultured for over 60 passages, has morphologic features like primary Müller cell (PMC) cultures and remains stable...
March 1, 2018: Investigative Ophthalmology & Visual Science
https://www.readbyqxmd.com/read/29625173/brain-mitochondrial-iron-accumulates-in-huntington-s-disease-mediates-mitochondrial-dysfunction-and-can-be-removed-pharmacologically
#13
Sonal Agrawal, Julia Fox, Baskaran Thyagarajan, Jonathan Fox
Mitochondrial bioenergetic dysfunction is involved in neurodegeneration in Huntington's disease (HD). Iron is critical for normal mitochondrial bioenergetics but can also contribute to pathogenic oxidation. The accumulation of iron in the brain occurs in mouse models and in human HD. Yet the role of mitochondria-related iron dysregulation as a contributor to bioenergetic pathophysiology in HD is unclear. We demonstrate here that human HD and mouse model HD (12-week R6/2 and 12-month YAC128) brains accumulated mitochondrial iron and showed increased expression of iron uptake protein mitoferrin 2 and decreased iron-sulfur cluster synthesis protein frataxin...
April 3, 2018: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/29625119/the-exosome-of-adipose-derived-stem-cells-reduces-%C3%AE-amyloid-pathology-and-apoptosis-of-neuronal-cells-derived-from-the-transgenic-mouse-model-of-alzheimer-s-disease
#14
Mijung Lee, Jae-Jun Ban, Seungwon Yang, Wooseok Im, Manho Kim
Adipose-derived stem cells (ADSC) have a therapeutic potential for the treatment of neurodegenerative disorders such as Alzheimer's disease (AD). Exosomes are extracellular vesicles secreted from various types of cells, and stem cell-derived exosomes are known to have beneficial effects in many diseases. Many studies have suggested that amyloid beta (Aβ) peptides have a pivotal role in AD progression, by mitochondrial dysfunction of neuronal cells. We examined the therapeutic potential of exosomes derived from ADSCs (ADSC-Exo) in preventing the disease phenotypes induced by the Aβ cascade in an AD in vitro model...
April 3, 2018: Brain Research
https://www.readbyqxmd.com/read/29624723/randomized-clinical-trial-of-rt001-early-signals-of-efficacy-in-friedreich-s-ataxia
#15
Theresa Zesiewicz, Frederic Heerinckx, Robert De Jager, Omid Omidvar, Marcus Kilpatrick, Jessica Shaw, Mikhail S Shchepinov
BACKGROUND: RT001 is a deuterated ethyl linoleate that inhibits lipid peroxidation and is hypothesized to reduce cellular damage and recover mitochondrial function in degenerative diseases such as Friedreich's ataxia. OBJECTIVE: To evaluate the safety, pharmacokinetics, and preliminary efficacy of RT001 in Friedreich's ataxia patients. DESIGN/METHODS: We conducted a phase I/II double-blind, comparator-controlled trial with 2 doses of RT001 in Friedreich's ataxia patients (9 subjects each cohort)...
April 6, 2018: Movement Disorders: Official Journal of the Movement Disorder Society
https://www.readbyqxmd.com/read/29623826/targeting-ampk-in-diabetes-and-diabetic-complications-energy-homeostasis-autophagy-and-mitochondrial-health
#16
Y V Madhavi, Nikhil Gaikwad, Veera Ganesh Yerra, Anil Kumar Kalvala, Srinivas Nanduri, Ashutosh Kumar
Adenosine 5'-monophosphate activated protein kinase (AMPK) is a key enzymatic protein involved in linking the energy sensing to the metabolic manipulation. It is a serine/threonine kinase activated by several upstream kinases. AMPK is a heterotrimeric protein complex regulated by AMP, ADP, and ATP allosterically. AMPK is ubiquitously expressed in various tissues of the living system such as heart, kidney, liver, brain and skeletal muscles. Thus malfunctioning of AMPK is expected to harbor several human pathologies especially diseases associated with metabolic and mitochondrial dysfunction...
April 6, 2018: Current Medicinal Chemistry
https://www.readbyqxmd.com/read/29618427/amelioration-of-methylmercury-induced-neural-damage-by-essential-oil-of-selinum-vaginatum-edgew-c-b-clarke
#17
Kalaivani Thiagarajan, Naisarg Gamit, Saurabh Mandal, Dhanoop Manikoth Ayyathan, Rajasekaran Chandrasekaran
Methylmercury (MeHg), an organometallic contaminant is a well spotted cause for a series of disorders, especially in the central nervous system. As there is no proper treatment, Selinum vaginatum (Edgew) C. B. Clarke, a traditional medicinal plant, is taken in the present study for assessing its neuroprotective effect against MeHg induced toxicity using rat brain mitochondrial fractions. The results of 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyltetrazolium bromide dye (MTT) assay indicated that there was a reduction in the mitochondrial viability in MeHg treated sample and IC50 value recorded was 2...
March 2018: Pakistan Journal of Pharmaceutical Sciences
https://www.readbyqxmd.com/read/29615062/kars-related-diseases-progressive-leukoencephalopathy-with-brainstem-and-spinal-cord-calcifications-as-new-phenotype-and-a-review-of-literature
#18
Anna Ardissone, Davide Tonduti, Andrea Legati, Eleonora Lamantea, Rita Barone, Imen Dorboz, Odile Boespflug-Tanguy, Gabriella Nebbia, Marco Maggioni, Barbara Garavaglia, Isabella Moroni, Laura Farina, Anna Pichiecchio, Simona Orcesi, Luisa Chiapparini, Daniele Ghezzi
BACKGROUND: KARS encodes lysyl- transfer ribonucleic acid (tRNA) synthetase, which catalyzes the aminoacylation of tRNA-Lys in the cytoplasm and mitochondria. Eleven families/sporadic patients and 16 different mutations in KARS have been reported to date. The associated clinical phenotype is heterogeneous ranging from early onset encephalopathy to isolated peripheral neuropathy or nonsyndromic hearing impairment. Recently additional presentations including leukoencephalopathy as predominant cerebral involvement or cardiomyopathy, isolated or associated with muscular and cerebral involvement, have been reported...
April 4, 2018: Orphanet Journal of Rare Diseases
https://www.readbyqxmd.com/read/29610859/the-mt-co1-v83i-polymorphism-is-a-risk-factor-for-primary-open-angle-glaucoma-in-african-american-men
#19
David W Collins, Harini V Gudiseva, Venkata R M Chavali, Benjamin Trachtman, Meera Ramakrishnan, William T Merritt Iii, Maxwell Pistilli, Rebecca A Rossi, Stephanie Blachon, Prithvi S Sankar, Eydie Miller-Ellis, Amanda Lehman, Victoria Addis, Joan M O'Brien
Purpose: We investigate the function of the V83I polymorphism (m.6150G>A, rs879053914) in the mitochondrial cytochrome c oxidase subunit 1 (MT-CO1) gene and its role in African American (AA) primary open-angle glaucoma (POAG). Methods: This study used Sanger sequencing (1339 cases, 850 controls), phenotypic characterization of Primary Open-Angle African American Glaucoma Genetics study (POAAGG) cases, a masked chart review of CO1 missense cases (V83I plus M117T, n = 29) versus wild type cases (n = 29), a yeast 2-hybrid (Y2H) cDNA library screen, and quantification of protein-protein interactions by Y2H and ELISA...
April 1, 2018: Investigative Ophthalmology & Visual Science
https://www.readbyqxmd.com/read/29609494/oxidative-damage-mediated-inos-and-ucp-2-upregulation-in-rat-brain-after-sub-acute-cyanide-exposure-dose-and-time-dependent-effects
#20
Rahul Bhattacharya, Poonam Singh, Jebin Jacob John, Niranjan L Gujar
Cyanide-induced chemical hypoxia is responsible for pronounced oxidative damage in the central nervous system. The disruption of mitochondrial oxidative metabolism has been associated with upregulation of uncoupling proteins (UCPs). The present study addresses the dose- and time-dependent effect of sub-acute cyanide exposure on various non-enzymatic and enzymatic oxidative stress markers and their correlation with inducible-nitric oxide synthase (iNOS) and uncoupling protein-2 (UCP-2) expression. Animals received (oral) triple distilled water (vehicle control), 0...
April 3, 2018: Drug and Chemical Toxicology
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