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https://www.readbyqxmd.com/read/29773580/resistin-inhibits-neuronal-autophagy-through-toll-like-receptor-4
#1
Jie Miao, Yacir Benomar, Sarah Al-Rifai, Ghislaine Poizat, Laure Riffault, Delphine Crepin, Mohammed Taouis
Autophagy is as a non-selective degradation pathway induced in energy-deprived cells and in non-starved cells by participating in cellular inflammatory responses mainly through the elimination of injured and aged mitochondria that constitute an important source of reactive oxygen species. We have previously reported that resistin/TLR4 signaling pathway induces inflammation and insulin resistance in neuronal cell. However, the impact of resistin-induced inflammation on neuronal autophagy is unknown. In the present study, we hypothesized that resistin-induced neuroinflammation could be attributed, at least partially, to the impairment of autophagy pathways in neuronal cells...
May 17, 2018: Journal of Endocrinology
https://www.readbyqxmd.com/read/29765861/mitochondrial-metabolism-mediated-regulation-of-adult-neurogenesis
#2
REVIEW
Ruth Beckervordersandforth
The life-long generation of new neurons from radial glia-like neural stem cells (NSCs) is achieved through a stereotypic developmental sequence that requires precise regulatory mechanisms to prevent exhaustion or uncontrolled growth of the stem cell pool. Cellular metabolism is the new kid on the block of adult neurogenesis research and the identity of stage-specific metabolic programs and their impact on neurogenesis turns out to be an emerging research topic in the field. Mitochondrial metabolism is best known for energy production but it contains a great deal more...
November 9, 2017: Brain Plasticity
https://www.readbyqxmd.com/read/29761302/cftr-prevents-neuronal-apoptosis-following-cerebral-ischemia-reperfusion-via-regulating-mitochondrial-oxidative-stress
#3
Ya-Ping Zhang, Yong Zhang, Zhi-Bin Xiao, Yan-Bo Zhang, Jing Zhang, Zhi-Qiang Li, Yao-Bin Zhu
The cystic fibrosis transmembrane conductance regulator (CFTR) is linked to cell apoptosis and abundantly expressed in brain tissue. Mitochondrial oxidative stress plays a key role in activating apoptotic pathway following cerebral ischemia reperfusion (IR) injury. Reduced glutathione (GSH) is exclusively synthesized in cytosol but distributed in mitochondria. In the present study, we investigated whether CFTR affected mitochondrial oxidative stress via regulating GSH and thereby protected neurons against apoptosis following cerebral IR...
May 14, 2018: Journal of Molecular Medicine: Official Organ of the "Gesellschaft Deutscher Naturforscher und Ärzte"
https://www.readbyqxmd.com/read/29760952/downregulation-of-the-psychiatric-susceptibility-gene-cacna1c-promotes-mitochondrial-resilience-to-oxidative-stress-in-neuronal-cells
#4
Susanne Michels, Goutham K Ganjam, Helena Martins, Gerhard M Schratt, Markus Wöhr, Rainer K W Schwarting, Carsten Culmsee
Affective disorders such as major depression and bipolar disorder are among the most prevalent forms of mental illness and their etiologies involve complex interactions between genetic and environmental risk factors. Over the past ten years, several genome wide association studies (GWAS) have identified CACNA1C as one of the strongest genetic risk factors for the development of affective disorders. However, its role in disease pathogenesis is still largely unknown. Vulnerability to affective disorders also involves diverse environmental risk factors such as perinatal insults, childhood maltreatment, and other adverse pathophysiological or psychosocial life events...
2018: Cell Death Discovery
https://www.readbyqxmd.com/read/29757281/analyses-of-mitochondrial-calcium-influx-in-isolated-mitochondria-and-cultured-cells
#5
Joshua T Maxwell, Chin-Hsien Tsai, Tahmina A Mohiuddin, Jennifer Q Kwong
Ca2+ handling by mitochondria is a critical function regulating both physiological and pathophysiological processes in a broad spectrum of cells. The ability to accurately measure the influx and efflux of Ca2+ from mitochondria is important for determining the role of mitochondrial Ca2+ handling in these processes. In this report, we present two methods for the measurement of mitochondrial Ca2+ handling in both isolated mitochondria and cultured cells. We first detail a plate reader-based platform for measuring mitochondrial Ca2+ uptake using the Ca2+ sensitive dye calcium green-5N...
April 27, 2018: Journal of Visualized Experiments: JoVE
https://www.readbyqxmd.com/read/29755410/mitochondrial-chaperones-in-the-brain-safeguarding-brain-health-and-metabolism
#6
José Pedro Castro, Kristina Wardelmann, Tilman Grune, André Kleinridders
The brain orchestrates organ function and regulates whole body metabolism by the concerted action of neurons and glia cells in the central nervous system. To do so, the brain has tremendously high energy consumption and relies mainly on glucose utilization and mitochondrial function in order to exert its function. As a consequence of high rate metabolism, mitochondria in the brain accumulate errors over time, such as mitochondrial DNA (mtDNA) mutations, reactive oxygen species, and misfolded and aggregated proteins...
2018: Frontiers in Endocrinology
https://www.readbyqxmd.com/read/29755319/ambra1-mediated-mitophagy-counteracts-oxidative-stress-and-apoptosis-induced-by-neurotoxicity-in-human-neuroblastoma-sh-sy5y-cells
#7
Anthea Di Rita, Pasquale D'Acunzo, Luca Simula, Silvia Campello, Flavie Strappazzon, Francesco Cecconi
Therapeutic strategies are needed to protect dopaminergic neurons in Parkinson's disease (PD) patients. Oxidative stress caused by dopamine may play an important role in PD pathogenesis. Selective autophagy of mitochondria (mitophagy), mainly regulated by PINK1 and PARKIN, plays an important role in the maintenance of cell homeostasis. Mutations in those genes cause accumulation of damaged mitochondria, leading to nigral degeneration and early-onset PD. AMBRA1ActA is a fusion protein specifically expressed at the mitochondria, and whose expression has been shown to induce a powerful mitophagy in mammalian cells...
2018: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/29751692/brain-mitochondria-aging-and-parkinson-s-disease
#8
REVIEW
Mario Rango, Nereo Bresolin
This paper reconsiders the role of mitochondria in aging and in Parkinson's Disease (PD). The most important risk factor for PD is aging. Alterations in mitochondrial activity are typical of aging. Mitochondrial aging is characterized by decreased oxidative phosphorylation, proteasome activity decrease, altered autophagy, and mitochondrial dysfunction. Beyond declined oxidative phosphorylation, mitochondrial dysfunction consists of a decline of beta-oxidation as well as of the Krebs cycle. Not inherited mitochondrial DNA (mtDNA) mutations are acquired over time and parallel the decrease in oxidative phosphorylation...
May 11, 2018: Genes
https://www.readbyqxmd.com/read/29748634/gene-by-environment-interactions-that-disrupt-mitochondrial-homeostasis-cause-neurodegeneration-in-c-elegans-parkinson-s-models
#9
Hanna Kim, Rylee J Perentis, Guy A Caldwell, Kim A Caldwell
Parkinson's disease (PD) is a complex multifactorial disorder where environmental factors interact with genetic susceptibility. Accumulating evidence suggests that mitochondria have a central role in the progression of neurodegeneration in sporadic and/or genetic forms of PD. We previously reported that exposure to a secondary metabolite from the soil bacterium, Streptomyces venezuelae, results in age- and dose-dependent dopaminergic (DA) neurodegeneration in Caenorhabditis elegans and human SH-SY5Y neurons...
May 10, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29748616/prion-protein-is-essential-for-the-re1-silencing-transcription-factor-rest-dependent-developmental-switch-in-synaptic-nmda-receptors
#10
Zhiqi Song, Wei Yang, Guangyu Cheng, Xiangmei Zhou, Lifeng Yang, Deming Zhao
It is important that the correct amounts of GluN2 subunits are maintained, as they determine NMDAR functional properties, which are crucial to neuronal communication, synaptogenesis and cognitive function. The transcriptional repressor RE1 silencing transcription factor (REST) is critical for the postnatal developmental switch in NMDARs. However, the mechanisms triggering REST and the link between NMDARs and REST are unclear. Here we show a new physiological essential role for cellular prion protein (PrPC ) in REST-dependent homeostasis and the developmental switch of NMDARs...
May 10, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29742958/mitochondrial-zn-2-accumulation-a-potential-trigger-of-hippocampal-ischemic-injury
#11
Sung G Ji, Yuliya V Medvedeva, Hwai-Lee Wang, Hong Z Yin, John H Weiss
Ischemic stroke is a major cause of death and disabilities worldwide, and it has been long hoped that improved understanding of relevant injury mechanisms would yield targeted neuroprotective therapies. While Ca2+ overload during ischemia-induced glutamate excitotoxicity has been identified as a major contributor, failures of glutamate targeted therapies to achieve desired clinical efficacy have dampened early hopes for the development of new treatments. However, additional studies examining possible contributions of Zn2+ , a highly prevalent cation in the brain, have provided new insights that may help to rekindle the enthusiasm...
May 1, 2018: Neuroscientist: a Review Journal Bringing Neurobiology, Neurology and Psychiatry
https://www.readbyqxmd.com/read/29742940/the-role-of-oxidative-stress-in-anxiety-disorder-cause-or-consequence
#12
Alessandra das Graças Fedoce, Frederico Ferreira, Robert G Bota, Vicent Bonet-Costa, Patrick Y Sun, Kelvin J A Davies
Anxiety disorders are the most common mental illness in the USA affecting 18% of the population. The cause(s) of anxiety disorders is/are not completely clear, and research in the neurobiology of anxiety at the molecular level is still rather limited. Although mounting clinical and preclinical evidence now indicates that oxidative stress may be a major component of anxiety pathology, whether oxidative stress is the cause or consequence remains elusive. Studies conducted over the past few years suggest that anxiety disorders may be characterized by lowered antioxidant defenses and increased oxidative damage to proteins, lipids and nucleic acids...
May 9, 2018: Free Radical Research
https://www.readbyqxmd.com/read/29742430/manipulation-of-mitochondria-dynamics-reveals-separate-roles-for-form-and-function-in-mitochondria-distribution
#13
Tatiana Trevisan, Diana Pendin, Aldo Montagna, Sergio Bova, Anna Maria Ghelli, Andrea Daga
Mitochondria shape is controlled by membrane fusion and fission mediated by mitofusins, Opa1, and Drp1, whereas mitochondrial motility relies on microtubule motors. These processes govern mitochondria subcellular distribution, whose defects are emphasized in neurons because of their polarized structure. We have studied how perturbation of the fusion/fission balance affects mitochondria distribution in Drosophila axons. Knockdown of Marf or Opa1 resulted in progressive loss of distal mitochondria and in a distinct oxidative phosphorylation and membrane potential deficit...
May 8, 2018: Cell Reports
https://www.readbyqxmd.com/read/29741354/extracellular-potassium-and-glutamate-interact-to-modulate-mitochondria-in-astrocytes
#14
Theresa S Rimmele, Haissa de Castro Abrantes, Joel Wellbourne-Wood, Sylvain Lengacher, Jean-Yves Chatton
Astrocytes clear glutamate and potassium, both of which are released into the extracellular space during neuronal activity. These processes are intimately linked with energy metabolism. Whereas astrocyte glutamate uptake causes cytosolic and mitochondrial acidification, extracellular potassium induces bicarbonate-dependent cellular alkalinization. This study aimed at quantifying the combined impact of glutamate and extracellular potassium on mitochondrial parameters of primary cultured astrocytes. Glutamate in 3mM potassium caused a stronger acidification of mitochondria compared to cytosol...
May 9, 2018: ACS Chemical Neuroscience
https://www.readbyqxmd.com/read/29732581/discrete-mitochondrial-aberrations-in-the-spinal-cord-of-sporadic-als-patients
#15
Vedad Delic, Crupa Kurien, Josean Cruz, Sandra Zivkovic, Jennifer Barretta, Avery Thomson, Daniel Hennessey, Jaheem Joseph, Jared Ehrhart, Alison E Willing, Patrick Bradshaw, Svitlana Garbuzova-Davis
Amyotrophic lateral sclerosis (ALS) is an adult onset neurodegenerative disease characterized by progressive motor neuron degeneration in the brain and spinal cord leading to muscle atrophy, paralysis, and death. Mitochondrial dysfunction is a major contributor to motor neuron degeneration associated with ALS progression. Mitochondrial abnormalities have been determined in spinal cords of animal disease models and ALS patients. However, molecular mechanisms leading to mitochondrial dysfunction in sporadic ALS (sALS) patients remain unclear...
May 6, 2018: Journal of Neuroscience Research
https://www.readbyqxmd.com/read/29719453/nobiletin-attenuates-neurotoxic-mitochondrial-calcium-overload-through-k-influx-and-%C3%AE-%C3%AE-m-across-mitochondrial-inner-membrane
#16
Ji Hyung Lee, Khulan Amarsanaa, Jinji Wu, Sang-Chan Jeon, Yanji Cui, Sung-Cherl Jung, Deok-Bae Park, Se-Jae Kim, Sang-Heon Han, Hyun-Wook Kim, Im Joo Rhyu, Su-Yong Eun
Mitochondrial calcium overload is a crucial event in determining the fate of neuronal cell survival and death, implicated in pathogenesis of neurodegenerative diseases. One of the driving forces of calcium influx into mitochondria is mitochondria membrane potential (ΔΨm ). Therefore, pharmacological manipulation of ΔΨm can be a promising strategy to prevent neuronal cell death against brain insults. Based on these issues, we investigated here whether nobiletin, a Citrus polymethoxylated flavone, prevents neurotoxic neuronal calcium overload and cell death via regulating basal ΔΨm against neuronal insult in primary cortical neurons and pure brain mitochondria isolated from rat cortices...
May 2018: Korean Journal of Physiology & Pharmacology
https://www.readbyqxmd.com/read/29718187/mutations-in-coa7-cause-spinocerebellar-ataxia-with-axonal-neuropathy
#17
Yujiro Higuchi, Ryuta Okunushi, Taichi Hara, Akihiro Hashiguchi, Junhui Yuan, Akiko Yoshimura, Kei Murayama, Akira Ohtake, Masahiro Ando, Yu Hiramatsu, Satoshi Ishihara, Hajime Tanabe, Yuji Okamoto, Eiji Matsuura, Takehiro Ueda, Tatsushi Toda, Sumimasa Yamashita, Kenichiro Yamada, Takashi Koide, Hiroaki Yaguchi, Jun Mitsui, Hiroyuki Ishiura, Jun Yoshimura, Koichiro Doi, Shinichi Morishita, Ken Sato, Masanori Nakagawa, Masamitsu Yamaguchi, Shoji Tsuji, Hiroshi Takashima
Several genes related to mitochondrial functions have been identified as causative genes of neuropathy or ataxia. Cytochrome c oxidase assembly factor 7 (COA7) may have a role in assembling mitochondrial respiratory chain complexes that function in oxidative phosphorylation. Here we identified four unrelated patients with recessive mutations in COA7 among a Japanese case series of 1396 patients with Charcot-Marie-Tooth disease (CMT) or other inherited peripheral neuropathies, including complex forms of CMT...
April 27, 2018: Brain: a Journal of Neurology
https://www.readbyqxmd.com/read/29715546/tdp-43-interacts-with-mitochondrial-proteins-critical-for-mitophagy-and-mitochondrial-dynamics
#18
Stephani A Davis, Sheed Itaman, Christopher M Khalid-Janney, Justin A Sherard, James A Dowell, Nigel J Cairns, Michael A Gitcho
Transactive response DNA-binding protein of 43 kDa (TDP-43) functions as a heterogeneous nuclear ribonucleoprotein and is the major pathological protein in frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis/motor neuron disease (ALS/MND). TDP-43 pathology may also be present as a comorbidity in approximately 20-50% of sporadic Alzheimer's disease cases. In a mouse model of MND, full-length TDP-43 increases association with the mitochondria and blocking the TDP-43/mitochondria interaction ameliorates motor dysfunction...
April 30, 2018: Neuroscience Letters
https://www.readbyqxmd.com/read/29710722/mitochondrial-dysfunction-as-a-predictor-and-driver-of-alzheimer-s-disease-like-pathology-in-oxys-rats
#19
Mikhail A Tyumentsev, Natalia A Stefanova, Natalia A Muraleva, Yulia V Rumyantseva, Elena Kiseleva, Valentin A Vavilin, Nataliya G Kolosova
Growing evidence suggests that mitochondrial dysfunction is an early event in sporadic Alzheimer's disease (AD), but the impact of mitochondrial dysfunction on the transition from healthy aging to AD remains elusive. Here we estimated the influence of mitochondrial dysfunction on the initiation of AD signs in OXYS rats, which simulate key characteristics of sporadic AD. We assessed the mitochondrial ultrastructure of pyramidal neurons of the hippocampus at the age preceding the development (age 20 days), during manifestation (4-5 months), and at the well-pronounced stages (18-24 months) of the AD-like pathology in OXYS rats...
April 27, 2018: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/29704317/development-of-gmp-1-a-molecular-chaperone-network-modulator-protecting-mitochondrial-function-and-its-assessment-in-fly-and-mice-models-of-alzheimer-s-disease
#20
Pavel F Pavlov, Birgit Hutter-Paier, Daniel Havas, Manfred Windisch, Bengt Winblad
Mitochondrial dysfunction is an early feature of Alzheimer's disease (AD) and may play an important role in the pathogenesis of disease. It has been shown that amyloid beta peptide (Aβ) and amyloid precursor protein (APP) interact with mitochondria contributing to the mitochondrial dysfunction in AD. Prevention of abnormal protein targeting to mitochondria can protect normal mitochondrial function, increase neuronal survival and at the end, ameliorate symptoms of AD and other neurodegenerative disorders. First steps of mitochondrial protein import are coordinated by molecular chaperones Hsp70 and Hsp90 that bind to the newly synthesized mitochondria-destined proteins and deliver them to the protein import receptors on the surface of organelle...
April 27, 2018: Journal of Cellular and Molecular Medicine
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