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reactive astrocyte

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https://www.readbyqxmd.com/read/29350438/astrocytic-glutamine-synthetase-is-expressed-in-the-neuronal-somatic-layers-and-down-regulated-proportionally-to-neuronal-loss-in-the-human-epileptic-hippocampus
#1
Ismini E Papageorgiou, Nektarios A Valous, Bernd Lahrmann, Hana Janova, Zin-Juan Klaft, Arend Koch, Ulf C Schneider, Peter Vajkoczy, Frank L Heppner, Niels Grabe, Niels Halama, Uwe Heinemann, Oliver Kann
Human mesial temporal lobe epilepsy (MTLE) features subregion-specific hippocampal neurodegeneration and reactive astrogliosis, including up-regulation of the glial fibrillary acidic protein (GFAP) and down-regulation of glutamine synthetase (GS). However, the regional astrocytic expression pattern of GFAP and GS upon MTLE-associated neurodegeneration still remains elusive. We assessed GFAP and GS expression in strict correlation with the local neuronal number in cortical and hippocampal surgical specimens from 16 MTLE patients using immunohistochemistry, stereology and high-resolution image analysis for digital pathology and whole-slide imaging...
January 19, 2018: Glia
https://www.readbyqxmd.com/read/29350434/the-cystine-glutamate-exchanger-xct-slc7a11-is-expressed-in-significant-concentrations-in-a-subpopulation-of-astrocytes-in-the-mouse-brain
#2
Sigrid Ottestad-Hansen, Qiu Xiang Hu, Virgine Veronique Follin-Arbelet, Eduard Bentea, Hideyo Sato, Ann Massie, Yun Zhou, Niels Christian Danbolt
The cystine-glutamate exchanger (xCT) promotes glutathione synthesis by catalyzing cystine uptake and glutamate release. The released glutamate may modulate normal neural signaling and contribute to excitotoxicity in pathological situations. Uncertainty, however, remains as neither the expression levels nor the distribution of xCT have been unambiguously determined. In fact, xCT has been reported in astrocytes, neurons, oligodendrocytes and microglia, but most of the information derives from cell cultures. Here, we show by immunohistochemistry and by Western blotting that xCT is widely expressed in the central nervous system of both sexes...
January 19, 2018: Glia
https://www.readbyqxmd.com/read/29349722/bystin-bysl-as-a-possible-marker-of-severe-hypoxic-ischemic-changes-in-neuropathological-examination-of-forensic-cases
#3
Mieszko Olczak, Dominik Chutorański, Magdalena Kwiatkowska, Dorota Samojłowicz, Sylwia Tarka, Teresa Wierzba-Bobrowicz
Bystin (BYSL) is a 306-amino acid protein encoded in humans by the BYSL gene located on the 6p21.1 chromosome. It is conserved across a wide range of eukaryotes. BYSL was reported to be a sensitive marker for the reactive astrocytes induced by ischemia/reperfusion and chemical hypoxia in vitro and is considered to be one of the common characteristics of astrogliosis. In our study we examined whether BYSL could be used as a marker for hypoxic-ischemic changes in forensic cases. Groups suspected of acute hypoxic-ischemic changes presented strong BYSL expression in the cytoplasm of neocortical neurons especially in layers 3-5, that seemed to be short-lasting...
January 18, 2018: Forensic Science, Medicine, and Pathology
https://www.readbyqxmd.com/read/29334986/bridging-pro-inflammatory-signals-synaptic-transmission-and-protection-in-spinal-explants-in-vitro
#4
M Medelin, V Giacco, A Aldinucci, G Castronovo, E Bonechi, A Sibilla, M Tanturli, M Torcia, L Ballerini, F Cozzolino, C Ballerini
Multiple sclerosis is characterized by tissue atrophy involving the brain and the spinal cord, where reactive inflammation contributes to the neurodegenerative processes. Recently, the presence of synapse alterations induced by the inflammatory responses was suggested by experimental and clinical observations, in experimental autoimmune encephalomyelitis mouse model and in patients, respectively. Further knowledge on the interplay between pro-inflammatory agents, neuroglia and synaptic dysfunction is crucial to the design of unconventional protective molecules...
January 15, 2018: Molecular Brain
https://www.readbyqxmd.com/read/29331305/tigar-inhibits-ischemia-reperfusion-induced-inflammatory-response-of-astrocytes
#5
Jieyu Chen, Ding-Mei Zhang, Xing Feng, Jian Wang, Yuan-Yuan Qin, Tian Zhang, Qiao Huang, Rui Sheng, Zhong Chen, Mei Li, Zheng-Hong Qin
The inflammatory response of glial cells contributes to neuronal damage or repair after brain ischemia/reperfusion insult. We previously demonstrated a protective role of TP53-induced glycolysis and apoptosis regulator (TIGAR) in ischemic neuronal injury through increasing the flow of pentose phosphate pathway (PPP). The present study investigated the possible role of TIGAR in ischemia/reperfusion-induced inflammatory response of astrocytes. Male ICR mice were subjected to middle cerebral artery occlusion for 2 h followed by 24 h reperfusion and cultured primary astrocytes were subjected to oxygen glucose deprivation for 9 h followed by 24 h reoxygenation (OGD/R)...
January 10, 2018: Neuropharmacology
https://www.readbyqxmd.com/read/29331263/glial-scars-are-permeable-to-the-neurotoxic-environment-of-chronic-stroke-infarcts
#6
Jacob C Zbesko, Thuy-Vi V Nguyen, Tao Yang, Jennifer Beischel Frye, Omar Hussain, Megan Hayes, Amanda Chung, W Anthony Day, Kristina Stepanovic, Maj Krumberger, Justine Mona, Frank M Longo, Kristian P Doyle
Following stroke, the damaged tissue undergoes liquefactive necrosis, a stage of infarct resolution that lasts for months, although the exact length of time is currently unknown. One method of repair involves reactive astrocytes and microglia forming a glial scar to compartmentalize the area of liquefactive necrosis from the rest of the brain. The formation of the glial scar is a critical component of the healing response to stroke, as well as other central nervous system (CNS) injuries. The goal of this study was to evaluate the toxicity of the extracellular fluid present in areas of liquefactive necrosis and determine how effectively it is segregated from the remainder of the brain...
January 10, 2018: Neurobiology of Disease
https://www.readbyqxmd.com/read/29323029/environmental-cues-determine-the-fate-of-astrocytes-after-spinal-cord-injury
#7
REVIEW
Fatima M Nathan, Shuxin Li
Reactive astrogliosis occurs after central nervous system (CNS) injuries whereby resident astrocytes form rapid responses along a graded continuum. Following CNS lesions, naïve astrocytes are converted into reactive astrocytes and eventually into scar-forming astrocytes that block axon regeneration and neural repair. It has been known for decades that scarring development and its related extracellular matrix molecules interfere with regeneration of injured axons after CNS injury, but the cellular and molecular mechanisms for controlling astrocytic scar formation and maintenance are not well known...
December 2017: Neural Regeneration Research
https://www.readbyqxmd.com/read/29315575/the-appswe-ps1a246e-mutations-in-an-astrocytic-cell-line-leads-to-increased-vulnerability-to-oxygen-and-glucose-deprivation-ca2-dysregulation-and-mitochondrial-abnormalities
#8
María Dolores Martin-de-Saavedra, Elisa Navarro, Ana J Moreno-Ortega, Mauricio P Cunha, Izaskun Buendia, Pablo Hernansanz-Agustín, Rafael León, María F Cano-Abad, Antonio Martínez-Ruiz, Ricardo Martínez-Murillo, Michael R Duchen, Manuela G López
Growing evidence suggests a close relationship between Alzheimer's Disease (AD) and cerebral hypoxia. Astrocytes play a key role in brain homeostasis and disease states, while some of the earliest changes in AD occur in astrocytes. We have therefore asked whether mutations associated with AD increase astrocyte vulnerability to ischemia. Two astroglioma cell lines derived from APPSWE /PS1A246E (APP, amyloid precursor protein; PS1, presenilin 1) transgenic mice and controls from normal mice were subjected to oxygen and glucose deprivation (OGD), an in vitro model of ischemia...
January 6, 2018: Journal of Neurochemistry
https://www.readbyqxmd.com/read/29305854/astrocytes-in-primary-cultures-express-serine-racemase-synthesize-d-serine-and-acquire-a1-reactive-astrocyte-features
#9
Suyan Li, Yota Uno, Uwe Rudolph, Johanna Cobb, Jing Liu, Thea Anderson, Deborah Levy, Darrick T Balu, Joseph T Coyle
D-Serine is a co-agonist at forebrain N-methyl-D-aspartate receptors (NMDAR) and is synthesized by serine racemase (SR). Although D-serine and SR were originally reported to be localized to glia, recent studies have provided compelling evidence that under healthy physiologic conditions both are localized primarily in neurons. However, in pathologic conditions, reactive astrocytes can also express SR and synthesize D-serine. Since cultured astrocytes exhibit features of reactive astrocytes, we have characterized D-serine synthesis and the expression of enzymes involved in its disposition in primary glial cultures...
January 3, 2018: Biochemical Pharmacology
https://www.readbyqxmd.com/read/29298427/the-aging-astrocyte-transcriptome-from-multiple-regions-of-the-mouse-brain
#10
Matthew M Boisvert, Galina A Erikson, Maxim N Shokhirev, Nicola J Allen
Aging brains undergo cognitive decline, associated with decreased neuronal synapse number and function and altered metabolism. Astrocytes regulate neuronal synapse formation and function in development and adulthood, but whether these properties change during aging, contributing to neuronal dysfunction, is unknown. We addressed this by generating aged and adult astrocyte transcriptomes from multiple mouse brain regions. These data provide a comprehensive RNA-seq database of adult and aged astrocyte gene expression, available online as a resource...
January 2, 2018: Cell Reports
https://www.readbyqxmd.com/read/29297157/astroglial-responses-to-amyloid-beta-progression-in-a-mouse-model-of-alzheimer-s-disease
#11
Malin Olsen, Ximena Aguilar, Dag Sehlin, Xiaotian T Fang, Gunnar Antoni, Anna Erlandsson, Stina Syvänen
PURPOSE: Alzheimer's disease (AD) is a neurodegenerative disorder characterized by amyloid-beta (Aβ) deposition, hyperphosphorylation of tau, and neuroinflammation. Astrocytes, the most abundant glial cell type in the nervous system, respond to neurodegenerative disorders through astrogliosis, i.e., converting to a reactive inflammatory state. The aim of this study was to investigate how in vivo quantification of astrogliosis using positron emission tomography (PET) radioligand deuterium-L-[11C]deprenyl ([11C]DED), binding to enzyme monoamine oxidase-B (MAO-B) which is overexpressed in reactive astrocytes during AD, corresponds to expression of glial fibrillary acidic protein (GFAP) and vimentin, i...
January 2, 2018: Molecular Imaging and Biology: MIB: the Official Publication of the Academy of Molecular Imaging
https://www.readbyqxmd.com/read/29284502/reciprocal-interactions-between-prostaglandin-e2-and-estradiol-dependent-signaling-pathways-in-the-injured-zebra-finch-brain
#12
Alyssa L Pedersen, Colin J Saldanha
BACKGROUND: Astrocytic aromatization and consequent increases in estradiol are neuroprotective in the injured brain. In zebra finches, cyclooxygenase-activity is necessary for injury-induced aromatase expression, and increased central estradiol lowers neuroinflammation. The mechanisms underlying these influences are unknown. Here, we document injury-induced, cyclooxygenase-dependent increases in glial aromatase expression and replicate previous work in our lab showing increases in central prostaglandin E2 and estradiol following brain damage...
December 29, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/29280091/the-gut-microbiome-in-neuromyelitis-optica
#13
REVIEW
Scott S Zamvil, Collin M Spencer, Sergio E Baranzini, Bruce A C Cree
Neuromyelitis optica (NMO) is a rare, disabling, sometimes fatal central nervous system inflammatory demyelinating disease that is associated with antibodies ("NMO IgG") that target the water channel protein aquaporin-4 (AQP4) expressed on astrocytes. There is considerable interest in identifying environmental triggers that may elicit production of NMO IgG by AQP4-reactive B cells. Although NMO is considered principally a humoral autoimmune disease, antibodies of NMO IgG are IgG1, a T-cell-dependent immunoglobulin subclass, indicating that AQP4-reactive T cells have a pivotal role in NMO pathogenesis...
December 26, 2017: Neurotherapeutics: the Journal of the American Society for Experimental NeuroTherapeutics
https://www.readbyqxmd.com/read/29279848/connexin43-and-ampk-have-essential-role-in-resistance-to-oxidative-stress-induced-necrosis
#14
Chunshan Zhao, Jinnv Fang, Chunguo Li, Min Zhang
Reactive oxygen species (ROS) induced oxidative stress leads to cell damage and neurological disorders in astrocytes. The gap junction protein connexin43 (Cx43) could form intercellular channels in astrocytes and the expression of Cx43 plays an important role in protecting the cells from damage. In the present study, we investigated the contribution of Cx43 to astrocytic necrosis induced by the ROS hydrogen peroxide (H2O2) and the mechanism by which AMPK was involved in this process. Fluorescence microscopy, flow cytometry, and western blot were used quantitatively and qualitatively to determine the cell apoptosis, necrosis, and protein expression...
2017: BioMed Research International
https://www.readbyqxmd.com/read/29279310/proliferating-ng2-cell-dependent-angiogenesis-and-scar-formation-alter-axon-growth-and-functional-recovery-after-spinal-cord-injury-in-mice
#15
Z C Hesp, R Y Yoseph, R Suzuki, C Wilson, A Nishiyama, D M McTigue
Spinal cord injury (SCI) induces a centralized fibrotic scar surrounded by a reactive glial scar at the lesion site. The origin of these scars is thought to be perivascular cells entering lesions on ingrowing blood vessels and reactive astrocytes, respectively. However, two NG2-expressing cell populations (pericytes and glia) also may influence scar formation. In the periphery, new blood vessel growth requires proliferating NG2+ pericytes; if also true in the CNS, then the fibrotic scar would depend on dividing NG2+ pericytes...
December 26, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/29274879/glial-cell-responses-in-a-murine-multifactorial-perinatal-brain-injury-model
#16
Miriam Domowicz, Natasha L Wadlington, Judith G Henry, Kasandra Diaz, Miranda J Munoz, Nancy B Schwartz
The impact of traumatic brain injury during the perinatal period, which coincides with glial cell (astrocyte and oligodendrocyte) maturation was assessed to determine whether a second insult, e.g., increased inflammation due to remote bacterial exposure, exacerbates the initial injury's effects, possibly eliciting longer-term brain damage. Thus, a murine multifactorial injury model incorporating both mechanisms consisting of perinatal penetrating traumatic brain injury, with or without intraperitoneal injection of lipopolysaccharide (LPS), an analog of remote pathogen exposure has been developed...
December 21, 2017: Brain Research
https://www.readbyqxmd.com/read/29274432/a-mouse-model-of-depdc5-related-epilepsy-neuronal-loss-of-depdc5-causes-dysplastic-and-ectopic-neurons-increased-mtor-signaling-and-seizure-susceptibility
#17
Christopher J Yuskaitis, Brandon M Jones, Rachel L Wolfson, Chloe E Super, Sameer C Dhamne, Alexander Rotenberg, David M Sabatini, Mustafa Sahin, Annapurna Poduri
DEPDC5 is a newly identified epilepsy-related gene implicated in focal epilepsy, brain malformations, and Sudden Unexplained Death in Epilepsy (SUDEP). In vitro, DEPDC5 negatively regulates amino acid sensing by the mTOR complex 1 (mTORC1) pathway, but the role of DEPDC5 in neurodevelopment and epilepsy has not been described. No animal model of DEPDC5-related epilepsy has recapitulated the neurological phenotypes seen in patients, and germline knockout rodent models are embryonic lethal. Here, we establish a neuron-specific Depdc5 conditional knockout mouse by cre-recombination under the Synapsin1 promotor...
December 20, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/29258870/delayed-neurochemical-effects-of-prenatal-exposure-to-mehg-in-the-cerebellum-of-developing-rats
#18
Luana Heimfarth, Jeferson Delgado, Moara Rodrigues Mingori, Karla Suzana Moresco, Regina Pessoa Pureur, Daniel Pens Gelain, José Cláudio Fonseca Moreira
Human fetuses and neonates are particularly vulnerable to methylmercury (MeHg)-induced brain damage and are sensitive even to low exposure levels. Previous work of our group evidence that prenatal exposure to MeHg causes cognitive and behavioral alterations and disrupt hippocampus signaling. The current study aimed to investigate the effect of gestational exposure of rats to MeHg at low doses (1 or 2 mg/Kg) on parameters of redox imbalance and key signaling pathways in the cerebellum of their offspring. Pregnant females received MeHg (treated group) or 0...
December 16, 2017: Toxicology Letters
https://www.readbyqxmd.com/read/29239336/neural-progenitor-cells-but-not-astrocytes-respond-distally-to-thoracic-spinal-cord-injury-in-rat-models
#19
Tara Nguyen, Yilin Mao, Theresa Sutherland, Catherine Anne Gorrie
Traumatic spinal cord injury (SCI) is a detrimental condition that causes loss of sensory and motor function in an individual. Many complex secondary injury cascades occur after SCI and they offer great potential for therapeutic targeting. In this study, we investigated the response of endogenous neural progenitor cells, astrocytes, and microglia to a localized thoracic SCI throughout the neuroaxis. Twenty-five adult female Sprague-Dawley rats underwent mild-contusion thoracic SCI (n = 9), sham surgery (n = 8), or no surgery (n = 8)...
November 2017: Neural Regeneration Research
https://www.readbyqxmd.com/read/29238610/a-role-for-erbb-signaling-in-the-induction-of-reactive-astrogliosis
#20
Jing Chen, Wanwan He, Xu Hu, Yuwen Shen, Junyan Cao, Zhengdong Wei, Yifei Luan, Li He, Fangdun Jiang, Yanmei Tao
Reactive astrogliosis is a hallmark of many neurological disorders, yet its functions and molecular mechanisms remain elusive. Particularly, the upstream signaling that regulates pathological responses of astrocytes is largely undetermined. We used a mouse traumatic brain injury model to induce astrogliosis and revealed activation of ErbB receptors in reactive astrocytes. Moreover, cell-autonomous inhibition of ErbB receptor activity in reactive astrocytes by a genetic approach suppressed hypertrophic remodeling possibly through the regulation of actin dynamics...
2017: Cell Discovery
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