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https://www.readbyqxmd.com/read/28440425/mitochondrial-transcription-factor-a-tfam-is-upregulated-in-glioma
#1
Hyunji Lee, Jisoo Park, Quangdon Tran, Dohoon Kim, Youngeun Hong, Hyeonjeong Cho, So Hee Kwon, Derek Brazil, Seon-Hwan Kim, Jongsun Park
Mitochondrial transcription factor A (TFAM), which was initially discovered as a transcription factor for mitochondrial DNA, has known to be critical for the regulation of mitochondrial DNA. However the possible involvement of TFAM in cancer is largely unknown. In this study, we have provided some evidence that TFAM may have a potential role in brain tumor. Western blot analysis with anti‑TFAM antibody indicated that TFAM is overexpressed in glioblastoma cell lines including U87MG and U251MG. Transcriptome profiling of U87MG and U251MG cells by using deep‑sequencing revealed that TFAM transcripts were upregulated in these cells compared to its of cerebral cortex...
April 12, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28438718/the-effect-of-50-compared-to-100-inspired-oxygen-fraction-on-brain-oxygenation-and-post-cardiac-arrest-mitochondrial-function-in-experimental-cardiac-arrest
#2
Annika Nelskyla, Jouni Nurmi, Milla Jousi, Alexey Schramko, Eero Mervaala, Giuseppe Ristagno, Markus B Skrifvars
BACKGROUND AND AIM: We hypothesised that the use of 50% compared to 100% oxygen maintains cerebral oxygenation and ameliorates the disturbance of cardiac mitochondrial respiration during cardiopulmonary resuscitation (CPR). METHODS: Ventricular fibrillation (VF) was induced electrically in anaesthetised healthy adult pigs and left untreated for seven minutes followed by randomisation to manual ventilation with 50% or 100% oxygen and mechanical chest compressions (LUCAS(®))...
April 21, 2017: Resuscitation
https://www.readbyqxmd.com/read/28438530/ferulic-acid-attenuates-brain-microvascular-endothelial-cells-damage-caused-by-oxygen-glucose-deprivation-via-punctate-mitochondria-dependent-mitophagy
#3
Jun-Li Chen, Wen-Jun Duan, Si Luo, Shi Li, Xiao-Hui Ma, Bo-Nan Hou, Shu-Yi Cheng, Shu-Huan Fang, Qi Wang, Shui-Qing Huang, Yun-Bo Chen
Ferulic acid (FA) has an important effect on scavenging free radicals, which is related to the alleviation of various neurodegenerative diseases. However, there are few studies about its effects on vascular dementia. In this study, we demonstrated the effect of FA on oxidative damage of brain microvascular endothelial cells (BMECs) which underwent oxygen-glucose deprivation (OGD) for 2 hours. Our data showed that FA significantly reversed the oxidative stress state of OGD-treated BMECs and reduced mitochondrial dysfunction...
April 21, 2017: Brain Research
https://www.readbyqxmd.com/read/28434975/protection-of-pc12%C3%A2-cells-from-cocaine-induced-cell-death-by-inhibiting-mitochondrial-permeability-transition
#4
Frederic Lamarche, Cecile Cottet-Rousselle, Luc Barret, Eric Fontaine
Cocaine abuse induces brain injury and neurodegeneration by a mechanism that has not yet been fully elucidated. Mitochondria play a key role in cell death processes, notably through the opening of the permeability transition pore (PTP). In this work, we examined the involvement of the PTP in cocaine-induced toxicity in PC12 cell lines. We used two different PTP inhibitors -i.e. cyclosporin A (CsA) and metformin-to assess their ability to counteract the cocaine induced effects. We first observed that a 48 h exposure to cocaine strongly sensitized cells to calcium overload, as measured by the calcium retention capacity...
April 20, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28434973/long-term-oral-kinetin-does-not-protect-against-%C3%AE-synuclein-induced-neurodegeneration-in-rodent-models-of-parkinson-s-disease
#5
Adam L Orr, Florentine U Rutaganira, Daniel de Roulet, Eric J Huang, Nicholas T Hertz, Kevan M Shokat, Ken Nakamura
Mutations in the mitochondrial kinase PTEN-induced putative kinase 1 (PINK1) cause Parkinson's disease (PD), likely by disrupting PINK1's kinase activity. Although the mechanism(s) underlying how this loss of activity causes degeneration remains unclear, increasing PINK1 activity may therapeutically benefit some forms of PD. However, we must first learn whether restoring PINK1 function prevents degeneration in patients harboring PINK1 mutations, or whether boosting PINK1 function can offer protection in more common causes of PD...
April 20, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28434655/apolipoprotein-e-receptors-and-modulation-of-alzheimer-s-disease
#6
REVIEW
Na Zhao, Chia-Chen Liu, Wenhui Qiao, Guojun Bu
Apolipoprotein E (apoE) is a lipid carrier in both the peripheral and the central nervous systems. Lipid-loaded apoE lipoprotein particles bind to several cell surface receptors to support membrane homeostasis and injury repair in the brain. Considering prevalence and relative risk magnitude, the ε4 allele of the APOE gene is the strongest genetic risk factor for late-onset Alzheimer's disease (AD). ApoE4 contributes to AD pathogenesis by modulating multiple pathways, including but not limited to the metabolism, aggregation, and toxicity of amyloid-β peptide, tauopathy, synaptic plasticity, lipid transport, glucose metabolism, mitochondrial function, vascular integrity, and neuroinflammation...
March 14, 2017: Biological Psychiatry
https://www.readbyqxmd.com/read/28434264/exploring-effects-of-remote-ischemic-preconditioning-in-a-pig-model-of-hypothermic-circulatory-arrest
#7
Johanna Herajärvi, Tuomas Anttila, Elitsa Y Dimova, Tuomas Laukka, Mikko Myllymäki, Henri Haapanen, Benjamin A Olenchock, Hannu Tuominen, Ulla Puistola, Peeter Karihtala, Kai Kiviluoma, Peppi Koivunen, Vesa Anttila, Tatu Juvonen
OBJECTIVES: During aortic and cardiac surgery, risks for mortality and morbidity are inevitable. Surgical setups involving deep hypothermic circulatory arrest (DHCA) are effective to achieve organ protection against ischemic injury. The aim of this study was to identify humoural factors mediating additive protective effects of remote ischemic preconditioning (RIPC) in a porcine model of DHCA. DESIGN: Twenty-two pigs were randomized into the RIPC group (n = 11) and the control group (n = 11)...
April 24, 2017: Scandinavian Cardiovascular Journal: SCJ
https://www.readbyqxmd.com/read/28433663/mitochondrial-mechanisms-of-neuronal-rescue-by-f-68-a-hydrophilic-pluronic-block-co-polymer-following-acute-substrate-deprivation
#8
REVIEW
Janice C Wang, Vytautas P Bindokas, Matthew Skinner, Todd Emrick, Jeremy D Marks
Global brain ischemia can lead to widespread neuronal death and poor neurologic outcomes in patients. Despite detailed understanding of the cellular and molecular mechanisms mediating neuronal death following focal and global brain hypoxia-ischemia, treatments to reduce ischemia-induced brain injury remain elusive. One pathway central to neuronal death following global brain ischemia is mitochondrial dysfunction, one consequence of which is the cascade of intracellular events leading to mitochondrial outer membrane permeabilization...
April 19, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28433458/linking-the-biological-underpinnings-of-depression-role-of-mitochondria-interactions-with-melatonin-inflammation-sirtuins-tryptophan-catabolites-dna-repair-and-oxidative-and-nitrosative-stress-with-consequences-for-classification-and-cognition
#9
REVIEW
George Anderson
The pathophysiological underpinnings of neuroprogressive processes in recurrent major depressive disorder (rMDD) are reviewed. A wide array of biochemical processes underlie MDD presentations and their shift to a recurrent, neuroprogressive course, including: increased immune-inflammation, tryptophan catabolites (TRYCATs), mitochondrial dysfunction, aryl hydrocarbonn receptor activation, and oxidative and nitrosative stress (O&NS), as well as decreased sirtuins and melatonergic pathway activity. These biochemical changes may have their roots in central, systemic and/or peripheral sites, including in the gut, as well as in developmental processes, such as prenatal stressors and breastfeeding consequences...
April 19, 2017: Progress in Neuro-psychopharmacology & Biological Psychiatry
https://www.readbyqxmd.com/read/28433109/pathogenesis-of-wilson-disease
#10
Ivo Florin Scheiber, Radan Brůha, Petr Dušek
Wilson disease is an autosomal-recessive disorder originating from a genetic defect in the copper-transporting ATPase ATP7B that is required for biliary copper secretion and loading of ceruloplasmin with copper. Impaired ATP7B function in Wilson disease results in excessive accumulation of copper in liver, brain, and other tissues. Toxic copper deposits may induce oxidative stress, modify expression of genes, directly inhibit proteins, and impair mitochondrial function, leading to hepatic, neuropsychiatric, renal, musculoskeletal, and other symptoms...
2017: Handbook of Clinical Neurology
https://www.readbyqxmd.com/read/28432362/succinate-supplementation-improves-metabolic-performance-of-mixed-glial-cell-cultures-with-mitochondrial-dysfunction
#11
Susan Giorgi-Coll, Ana I Amaral, Peter J A Hutchinson, Mark R Kotter, Keri L H Carpenter
Mitochondrial dysfunction, the inability to efficiently utilise metabolic fuels and oxygen, contributes to pathological changes following traumatic spinal cord or traumatic brain injury (TBI). In the present study, we tested the hypothesis that succinate supplementation can improve cellular energy state under metabolically stressed conditions in a robust, reductionist in vitro model of mitochondrial dysfunction in which primary mixed glial cultures (astrocytes, microglia and oligodendrocytes) were exposed to the mitochondrial complex I inhibitor rotenone...
April 21, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28432298/endogenous-two-photon-excited-fluorescence-imaging-characterizes-neuron-and-astrocyte-metabolic-responses-to-manganese-toxicity
#12
Emily Stuntz, Yusi Gong, Disha Sood, Volha Liaudanskaya, Dimitra Pouli, Kyle P Quinn, Carlo Alonzo, Zhiyi Liu, David L Kaplan, Irene Georgakoudi
As neurodegenerative conditions are increasingly linked to mitochondrial dysfunction, methods for studying brain cell metabolism at high spatial resolution are needed to elucidate neurodegeneration mechanisms. Two-photon excited fluorescence (TPEF) imaging is a non-destructive, high-resolution technique for studying cell metabolism via endogenous fluorescence of reduced nicotinamide adenine dinucleotide (phosphate) (NAD(P)H) and flavin adenine dinucleotide (FAD). We employed TPEF to study the metabolism of primary rat astrocyte and neuronal cultures under normal growth conditions and in response to manganese (Mn) treatment...
April 21, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28432138/inhibition-of-drp1-ameliorates-synaptic-depression-a%C3%AE-deposition-and-cognitive-impairment-in-alzheimer-s-disease-model
#13
Seung-Hyun Baek, So Jung Park, Jae In Jeong, Sung Hyun Kim, Jihoon Han, Jae Won Kyung, Sang-Ha Baik, Yuri Choi, Bo-Youn Choi, Jinsu Park, Gahee Bahn, Ji Hyun Shin, Doo Sin Jo, Joo-Yong Lee, Choon-Gon Jang, Thiruma V Arumugam, Jongpil Kim, Jeung-Whan Han, Jae-Young Koh, Dong-Hyung Cho, Dong-Gyu Jo
Excessive mitochondrial fission is a prominent early event, and contributes to mitochondrial dysfunction, synaptic failure and neuronal cell death in the progression of Alzheimer's disease (AD). However, it remains to be determined whether inhibition of excessive mitochondrial fission is beneficial in mammal models of AD. To determine whether dynamin-related protein 1 (Drp1), a key regulator of mitochondrial fragmentation, can be a disease-modifying therapeutic target for AD, we examine the effects of Drp1 inhibitor on mitochondrial and synaptic dysfunctions induced by oligomeric β-amyloid (Aβ) in neurons, and neuropathology and cognitive functions in APP/PS1 double transgenic AD mice...
April 21, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28431972/mitochondrial-energy-metabolism-of-rat-hippocampus-after-treatment-with-the-antidepressants-desipramine-and-fluoxetine
#14
Roberto Federico Villa, Federica Ferrari, Laura Bagini, Antonella Gorini, Nicoletta Brunello, Fabio Tascedda
Alterations in mitochondrial functions have been hypothesized to participate in the pathogenesis of depression, because brain bioenergetic abnormalities have been detected in depressed patients by neuroimaging in vivo studies. However, this hypothesis is not clearly demonstrated in experimental studies: some suggest that antidepressants are inhibitors of mitochondrial metabolism, while others observe the opposite. In this study, the effects of 21-day treatment with desipramine (15 mg/kg) and fluoxetine (10 mg/kg) were examined on the energy metabolism of rat hippocampus, evaluating the catalytic activity of regulatory enzymes of mitochondrial energy-yielding metabolic pathways...
April 18, 2017: Neuropharmacology
https://www.readbyqxmd.com/read/28430993/a-multi-systemic-mitochondrial-disorder-due-to-a-dominant-p-y955h-disease-variant-in-dna-polymerase-gamma
#15
Triinu Siibak, Paula Clemente, Ana Bratic, Helene Bruhn, Timo E S Kauppila, Bertil Macao, Florian A Schober, Nicole Lesko, Rolf Wibom, Karin Naess, Inger Nennesmo, Anna Wedell, Bradley Peter, Christoph Freyer, Maria Falkenberg, Anna Wredenberg
Mutations in the mitochondrial DNA polymerase, POLG, are associated with a variety of clinical presentations, ranging from early onset fatal brain disease in Alpers syndrome to chronic progressive external ophthalmoplegia. The majority of mutations are linked with disturbances of mitochondrial DNA (mtDNA) integrity and maintenance. On a molecular level, depending on their location within the enzyme, mutations either lead to mtDNA depletion or the accumulation of multiple mtDNA deletions, and in some cases these molecular changes can be correlated to the clinical presentation...
April 17, 2017: Human Molecular Genetics
https://www.readbyqxmd.com/read/28429368/-aralar-agc1-deficiency-a-neurodevelopmental-disorder-with-severe-impairment-of-neuronal-mitochondrial-respiration-does-not-produce-a-primary-increase-in-brain-lactate
#16
Inés Juaristi, María L García-Martin, Tiago B Rodrigues, Jorgina Satrústegui, Irene Llorente-Folch, Beatriz Pardo
ARALAR/AGC1 (aspartate-glutamate mitochondrial carrier 1) is an important component of the NADH malate-aspartate shuttle (MAS). AGC1-deficiency is a rare disease causing global cerebral hypomyelination, developmental arrest, hypotonia, and epilepsy (OMIM ID #612949); the aralar-KO mouse recapitulates the major findings in humans. This study was aimed at understanding the impact of ARALAR-deficiency in brain lactate levels as a biomarker. We report that lactate was equally abundant in wild-type and aralar-KO mouse brain in vivo at PND 17...
April 21, 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/28427446/respiratory-chain-complex-iii-deficiency-due-to-mutated-bcs1l-a-novel-phenotype-with-encephalomyopathy-partially-phenocopied-in-a-bcs1l-mutant-mouse-model
#17
Saara Tegelberg, Nikica Tomašić, Jukka Kallijärvi, Janne Purhonen, Eskil Elmér, Eva Lindberg, David Gisselsson Nord, Maria Soller, Nicole Lesko, Anna Wedell, Helene Bruhn, Christoph Freyer, Henrik Stranneheim, Rolf Wibom, Inger Nennesmo, Anna Wredenberg, Erik A Eklund, Vineta Fellman
BACKGROUND: Mitochondrial diseases due to defective respiratory chain complex III (CIII) are relatively uncommon. The assembly of the eleven-subunit CIII is completed by the insertion of the Rieske iron-sulfur protein, a process for which BCS1L protein is indispensable. Mutations in the BCS1L gene constitute the most common diagnosed cause of CIII deficiency, and the phenotypic spectrum arising from mutations in this gene is wide. RESULTS: A case of CIII deficiency was investigated in depth to assess respiratory chain function and assembly, and brain, skeletal muscle and liver histology...
April 20, 2017: Orphanet Journal of Rare Diseases
https://www.readbyqxmd.com/read/28422384/natural-antioxidant-flavonoids-in-formalin-induced-mice-paw-inflammation-inhibition-of-mitochondrial-sorbitol-dehydrogenase-activity
#18
Ebtehal Mohammad F, Wedad A Hasan, Eman G Mohamed
Flavonoids have reported to cover interesting multiple pharmacological properties. This study evaluated the effect of apigenin or silymarin in paw inflammation induced by formalin in mice. Mice were divided into four groups: I: positive control group; II: apigenin, 3 mg/kg (i.p.); III: silymarin 50 mg/kg (p.o.); IV: meloxicam 10 mg/kg (p.o.), the reference drug. Therapies were administered once a day for 7 days. The curative effects were assessed on inflammatory, oxidative stress and neurotransmitter biomarkers, and apoptosis...
April 19, 2017: Journal of Biochemical and Molecular Toxicology
https://www.readbyqxmd.com/read/28420982/tau-oligomers-cytotoxicity-propagation-and-mitochondrial-damage
#19
REVIEW
Scott S Shafiei, Marcos J Guerrero-Muñoz, Diana L Castillo-Carranza
Aging has long been considered as the main risk factor for several neurodegenerative disorders including a large group of diseases known as tauopathies. Even though neurofibrillary tangles (NFTs) have been examined as the main histopathological hallmark, they do not seem to play a role as the toxic entities leading to disease. Recent studies suggest that an intermediate form of tau, prior to NFT formation, the tau oligomer, is the true toxic species. However, the mechanisms by which tau oligomers trigger neurodegeneration remain unknown...
2017: Frontiers in Aging Neuroscience
https://www.readbyqxmd.com/read/28420091/dietary-sugars-and-endogenous-formation-of-advanced-glycation-endproducts-emerging-mechanisms-of-disease
#20
REVIEW
Manuela Aragno, Raffaella Mastrocola
The rapid increase in metabolic diseases, which occurred in the last three decades in both industrialized and developing countries, has been related to the rise in sugar-added foods and sweetened beverages consumption. An emerging topic in the pathogenesis of metabolic diseases related to modern nutrition is the role of Advanced Glycation Endproducts (AGEs). AGEs can be ingested with high temperature processed foods, but also endogenously formed as a consequence of a high dietary sugar intake. Animal models of high sugar consumption, in particular fructose, have reported AGE accumulation in different tissues in association with peripheral insulin resistance and lipid metabolism alterations...
April 14, 2017: Nutrients
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