4,073 results match your criteria Glia [Journal]


Independent and cooperative roles of the Mek/ERK1/2-MAPK and PI3K/Akt/mTOR pathways during developmental myelination and in adulthood.

Glia 2019 Feb 13. Epub 2019 Feb 13.

Department of Neuroscience, University of Connecticut Medical School, Farmington, Connecticut, USA.

Multiple extracellular and intracellular signals regulate the functions of oligodendrocytes as they progress through the complex process of developmental myelination and then maintain a functionally intact myelin sheath throughout adult life, preserving the integrity of the axons. Recent studies suggest that Mek/ERK1/2-MAPK and PI3K/Akt/mTOR intracellular signaling pathways play important, often overlapping roles in the regulation of myelination. However, it remains poorly understood whether they function independently, sequentially, or converge using a common mechanism to facilitate oligodendrocyte differentiation, myelin growth, and maintenance. Read More

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http://dx.doi.org/10.1002/glia.23602DOI Listing
February 2019

A core transcriptional signature of human microglia: Derivation and utility in describing region-dependent alterations associated with Alzheimer's disease.

Glia 2019 Feb 13. Epub 2019 Feb 13.

The Roslin Institute, University of Edinburgh, Easter Bush, Midlothian, Scotland, United Kingdom.

Growing recognition of the pivotal role microglia play in neurodegenerative and neuroinflammatory disorders has accentuated the need to characterize their function in health and disease. Studies in mouse have applied transcriptome-wide profiling of microglia to reveal key features of microglial ontogeny, functional profile, and phenotypic diversity. While similar, human microglia exhibit clear differences to their mouse counterparts, underlining the need to develop a better understanding of the human microglial profile. Read More

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http://dx.doi.org/10.1002/glia.23572DOI Listing
February 2019

LRP1 deficiency in microglia blocks neuro-inflammation in the spinal dorsal horn and neuropathic pain processing.

Glia 2019 Feb 11. Epub 2019 Feb 11.

Department of Pathology, University of California San Diego, La Jolla, California.

Following injury to the peripheral nervous system (PNS), microglia in the spinal dorsal horn (SDH) become activated and contribute to the development of local neuro-inflammation, which may regulate neuropathic pain processing. The molecular mechanisms that control microglial activation and its effects on neuropathic pain remain incompletely understood. We deleted the gene encoding the plasma membrane receptor, LDL Receptor-related Protein-1 (LRP1), conditionally in microglia using two distinct promoter-Cre recombinase systems in mice. Read More

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http://dx.doi.org/10.1002/glia.23599DOI Listing
February 2019

Mechano-modulation of nuclear events regulating oligodendrocyte progenitor gene expression.

Glia 2019 Feb 8. Epub 2019 Feb 8.

Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, New York.

Oligodendrocytes differentiate from oligodendrocyte progenitor cells (OPCs) in response to distinct extracellular signals. This process requires changes in gene expression resulting from the interplay between transcription factors and epigenetic modulators. Extracellular signals include chemical and physical stimuli. Read More

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http://dx.doi.org/10.1002/glia.23595DOI Listing
February 2019

A gene regulatory architecture that controls region-independent dynamics of oligodendrocyte differentiation.

Glia 2019 Feb 7. Epub 2019 Feb 7.

Laboratory of Systems Tumor Immunology, Hautklinik, Universitätsklinikum Erlangen and Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany.

Oligodendrocytes (OLs) facilitate information processing in the vertebrate central nervous system via axonal ensheathment. The structure and dynamics of the regulatory network that mediates oligodendrogenesis are poorly understood. We employed bioinformatics and meta-analysis of high-throughput datasets to reconstruct a regulatory network underpinning OL differentiation. Read More

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http://dx.doi.org/10.1002/glia.23569DOI Listing
February 2019

Structurally defined signaling in neuro-glia units in the enteric nervous system.

Glia 2019 Feb 7. Epub 2019 Feb 7.

Laboratory for Enteric NeuroScience (LENS), Translational Research Center for Gastrointestinal Disorders (TARGID), University of Leuven, Leuven, Belgium.

Coordination of gastrointestinal function relies on joint efforts of enteric neurons and glia, whose crosstalk is vital for the integration of their activity. To investigate the signaling mechanisms and to delineate the spatial aspects of enteric neuron-to-glia communication within enteric ganglia we developed a method to stimulate single enteric neurons while monitoring the activity of neighboring enteric glial cells. We combined cytosolic calcium uncaging of individual enteric neurons with calcium imaging of enteric glial cells expressing a genetically encoded calcium indicator and demonstrate that enteric neurons signal to enteric glial cells through pannexins using paracrine purinergic pathways. Read More

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http://dx.doi.org/10.1002/glia.23596DOI Listing
February 2019

Early embryonic NG2 glia are exclusively gliogenic and do not generate neurons in the brain.

Glia 2019 Feb 6. Epub 2019 Feb 6.

Molecular Physiology, Center for Integrative Physiology and Molecular Medicine (CIPMM), University of Saarland, Homburg, Germany.

In the central nervous system, the type I transmembrane glycoprotein NG2 (nerve-glia antigen 2) is only expressed by pericytes and oligodendrocyte precursor cells (OPCs). Therefore, OPCs are also termed NG2 glia. Their fate during development has been investigated systematically in several genetically modified mouse models. Read More

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http://dx.doi.org/10.1002/glia.23590DOI Listing
February 2019
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Glial TLR2-driven innate immune responses and CD8 T cell activation against brain tumor.

Glia 2019 Feb 5. Epub 2019 Feb 5.

Immunotherapeutics Branch, National Cancer Center, Goyang, South Korea.

Growing interest has been focused on the roles of microglia as sentinels and effector cells that guard diverse pathological milieu in the brain. Here, it has been reported that microglial TLR2 is a crucial molecule that confers innate and adaptive immunity against brain tumor. TLR2 is preferentially expressed on microglia, brain-resident immune cells, in the tumor-bearing cerebral hemisphere of mouse and rat intracranial tumor models. Read More

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http://dx.doi.org/10.1002/glia.23597DOI Listing
February 2019
6.031 Impact Factor

Gap junction mediated signaling between satellite glia and neurons in trigeminal ganglia.

Glia 2019 Feb 4. Epub 2019 Feb 4.

Laboratory of Experimental Surgery, Department of Surgery, Hadassah-Hebrew University Medical Center, Jerusalem, Israel.

Peripheral sensory ganglia contain the somata of neurons mediating mechanical, thermal, and painful sensations from somatic, visceral, and oro-facial organs. Each neuronal cell body is closely surrounded by satellite glial cells (SGCs) that have properties and functions similar to those of central astrocytes, including expression of gap junction proteins and functional dye coupling. As shown in other pain models, after systemic pain induction by intra-peritoneal injection of lipopolysaccharide, dye coupling among SGCs in intact trigeminal ganglion was enhanced. Read More

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http://dx.doi.org/10.1002/glia.23554DOI Listing
February 2019
1 Read

Chronic neurodegeneration induces type I interferon synthesis via STING, shaping microglial phenotype and accelerating disease progression.

Glia 2019 Jan 25. Epub 2019 Jan 25.

School of Biochemistry and Immunology, Trinity College Institute of Neuroscience & Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Republic of Ireland.

Type I interferons (IFN-I) are the principal antiviral molecules of the innate immune system and can be made by most cell types, including central nervous system cells. IFN-I has been implicated in neuroinflammation during neurodegeneration, but its mechanism of induction and its consequences remain unclear. In the current study, we assessed expression of IFN-I in murine prion disease (ME7) and examined the contribution of the IFN-I receptor IFNAR1 to disease progression. Read More

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http://dx.doi.org/10.1002/glia.23592DOI Listing
January 2019
6.031 Impact Factor

Importance of GFAP isoform-specific analyses in astrocytoma.

Glia 2019 Jan 22. Epub 2019 Jan 22.

Department of Translational Neuroscience, Brain Center Rudolf Magnus, University Medical Center Utrecht, Utrecht University, Heidelberglaan 100, 3584 CX, Utrecht, The Netherlands.

Gliomas are a heterogenous group of malignant primary brain tumors that arise from glia cells or their progenitors and rely on accurate diagnosis for prognosis and treatment strategies. Although recent developments in the molecular biology of glioma have improved diagnosis, classical histological methods and biomarkers are still being used. The glial fibrillary acidic protein (GFAP) is a classical marker of astrocytoma, both in clinical and experimental settings. Read More

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http://dx.doi.org/10.1002/glia.23594DOI Listing
January 2019
1 Read

The PTN-PTPRZ signal activates the AFAP1L2-dependent PI3K-AKT pathway for oligodendrocyte differentiation: Targeted inactivation of PTPRZ activity in mice.

Glia 2019 Jan 22. Epub 2019 Jan 22.

Division of Molecular Neurobiology, National Institute for Basic Biology (NIBB), Okazaki, Aichi, Japan.

Protein tyrosine phosphatase receptor type Z (PTPRZ) maintains oligodendrocyte precursor cells (OPCs) in an undifferentiated state. The inhibition of PTPase by its ligand pleiotrophin (PTN) promotes OPC differentiation; however, the substrate molecules of PTPRZ involved in the differentiation have not yet been elucidated in detail. We herein demonstrated that the tyrosine phosphorylation of AFAP1L2, paxillin, ERBB4, GIT1, p190RhoGAP, and NYAP2 was enhanced in OPC-like OL1 cells by a treatment with PTN. Read More

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http://dx.doi.org/10.1002/glia.23583DOI Listing
January 2019

Blockade of microglial adenosine A receptor suppresses elevated pressure-induced inflammation, oxidative stress, and cell death in retinal cells.

Glia 2019 Jan 22. Epub 2019 Jan 22.

Coimbra Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, University of Coimbra, Coimbra, Portugal.

Glaucoma is a retinal degenerative disease characterized by the loss of retinal ganglion cells and damage of the optic nerve. Recently, we demonstrated that antagonists of adenosine A receptor (A R) control retinal inflammation and afford protection to rat retinal cells in glaucoma models. However, the precise contribution of microglia to retinal injury was not addressed, as well as the effect of A R blockade directly in microglia. Read More

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http://dx.doi.org/10.1002/glia.23579DOI Listing
January 2019
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In vivo Ca imaging of astrocytic microdomains reveals a critical role of the amyloid precursor protein for mitochondria.

Glia 2019 Jan 22. Epub 2019 Jan 22.

Division of Translational Brain Research, German Center for Neurodegenerative Diseases (DZNE), Munich, Germany.

The investigation of amyloid precursor protein (APP) has been mainly confined to its neuronal functions, whereas very little is known about its physiological role in astrocytes. Astrocytes exhibit a particular morphology with slender extensions protruding from somata and primary branches. Along these fine extensions, spontaneous calcium transients occur in spatially restricted microdomains. Read More

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http://dx.doi.org/10.1002/glia.23584DOI Listing
January 2019

Chronic pain induces nociceptive neurogenesis in dorsal root ganglia from Sox2-positive satellite cells.

Glia 2019 Jan 16. Epub 2019 Jan 16.

Department of Neurobiology, Institute of Neurosciences, School of Basic Medicine, Fourth Military Medical University, Xi'an, Shaanxi, China.

Chronic pain is one of the most prevalent chronic diseases in the world. The plastic changes of sensory neurons in dorsal root ganglia (DRG) have been extensively studied as the underlying periphery mechanism. Recent studies revealed that satellite cells, the major glial cells in DRG, also played important roles in the development/modulation of chronic pain. Read More

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http://dx.doi.org/10.1002/glia.23588DOI Listing
January 2019
2 Reads

Lysophosphatidic acid activates satellite glia cells and Schwann cells.

Glia 2019 Jan 13. Epub 2019 Jan 13.

Institute of Physiology and Pathophysiology, Friedrich-Alexander-University of Erlangen-Nürnberg, Erlangen, Germany.

Pruritus is a common and disabling symptom in patients with hepatobiliary disorders, particularly in those with cholestatic features. Serum levels of lysophosphatidic acid (LPA) and its forming enzyme autotaxin were increased in patients suffering from hepatic pruritus, correlated with itch severity and response to treatment. Here we show that in a culture of dorsal root ganglia LPA 18:1 surprisingly activated a large fraction of satellite glia cells, and responses to LPA 18:1 correlated inversely with responses to neuronal expressed transient receptor potential channels. Read More

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http://dx.doi.org/10.1002/glia.23585DOI Listing
January 2019

Lipopolysaccharide-induced alteration of mitochondrial morphology induces a metabolic shift in microglia modulating the inflammatory response in vitro and in vivo.

Glia 2019 Jan 13. Epub 2019 Jan 13.

Centre of Perinatal Medicine and Health, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.

Accumulating evidence suggests that changes in the metabolic signature of microglia underlie their response to inflammation. We sought to increase our knowledge of how pro-inflammatory stimuli induce metabolic changes. Primary microglia exposed to lipopolysaccharide (LPS)-expressed excessive fission leading to more fragmented mitochondria than tubular mitochondria. Read More

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http://doi.wiley.com/10.1002/glia.23587
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http://dx.doi.org/10.1002/glia.23587DOI Listing
January 2019
5 Reads

Direct conversion of adult human skin fibroblasts into functional Schwann cells that achieve robust recovery of the severed peripheral nerve in rats.

Glia 2019 Jan 13. Epub 2019 Jan 13.

Department of Stem Cell Biology and Histology, Tohoku University Graduate School of Medicine, Sendai, Japan.

Direct conversion is considered a promising approach to obtain tissue-specific cells for cell therapies; however, this strategy depends on exogenous gene expression that may cause undesired adverse effects such as tumorigenesis. By optimizing the Schwann cell induction system, which was originally developed for trans-differentiation of bone marrow mesenchymal stem cells into Schwann cells, we established a system to directly convert adult human skin fibroblasts into cells comparable to authentic human Schwann cells without gene introduction. Serial treatments with beta-mercaptoethanol, retinoic acid, and finally a cocktail of basic fibroblast growth factor, forskolin, platelet-derived growth factor-AA, and heregulin-β1 (EGF domain) converted fibroblasts into cells expressing authentic Schwann cell markers at an efficiency of approximately 75%. Read More

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http://doi.wiley.com/10.1002/glia.23582
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http://dx.doi.org/10.1002/glia.23582DOI Listing
January 2019
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Maintenance of high proteolipid protein level in adult central nervous system myelin is required to preserve the integrity of myelin and axons.

Glia 2019 Jan 14. Epub 2019 Jan 14.

Department of Neurogenetics, Max Planck Institute of Experimental Medicine, Göttingen, Germany.

Proteolipid protein (PLP) is the most abundant integral membrane protein in central nervous system (CNS) myelin. Expression of the Plp-gene in oligodendrocytes is not essential for the biosynthesis of myelin membranes but required to prevent axonal pathology. This raises the question whether the exceptionally high level of PLP in myelin is required later in life, or whether high-level PLP expression becomes dispensable once myelin has been assembled. Read More

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http://dx.doi.org/10.1002/glia.23549DOI Listing
January 2019
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ErbB receptor signaling directly controls oligodendrocyte progenitor cell transformation and spontaneous remyelination after spinal cord injury.

Glia 2019 Jan 13. Epub 2019 Jan 13.

King's College London, Regeneration Group, The Wolfson Centre for Age-Related Diseases, Institute of Psychiatry, Psychology & Neuroscience (IoPPN), London, United Kingdom.

We recently discovered a novel role for neuregulin-1 (Nrg1) signaling in mediating spontaneous regenerative processes and functional repair after spinal cord injury (SCI). We revealed that Nrg1 is the molecular signal responsible for spontaneous functional remyelination of dorsal column axons by peripheral nervous system (PNS)-like Schwann cells after SCI. Here, we investigate whether Nrg1/ErbB signaling controls the unusual transformation of centrally derived progenitor cells into these functional myelinating Schwann cells after SCI using a fate-mapping/lineage tracing approach. Read More

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http://dx.doi.org/10.1002/glia.23586DOI Listing
January 2019
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Regionally selective knockdown of astroglial glutamate transporters in infralimbic cortex induces a depressive phenotype in mice.

Glia 2019 Jan 11. Epub 2019 Jan 11.

Department of Neurochemistry and Neuropharmacology, Instituto de Investigaciones Biomédicas de Barcelona (IIBB - CSIC), Barcelona, Spain.

Elevation of energy metabolism and disturbance of astrocyte number/function in the ventral anterior cingulate cortex (vACC) contributes to the pathophysiology of major depressive disorder (MDD). Functional hyperactivity of vACC may result from reduced astrocytic glutamate uptake and increased neuronal excitation. Here we tested this hypothesis by knocking-down astrocytic glutamate transporter GLAST/GLT-1 expression in mouse infralimbic (IL, rodent equivalent of vACC) or prelimbic (PrL) cortices using RNAi strategies. Read More

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http://doi.wiley.com/10.1002/glia.23593
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http://dx.doi.org/10.1002/glia.23593DOI Listing
January 2019
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Repair Schwann cell update: Adaptive reprogramming, EMT, and stemness in regenerating nerves.

Glia 2019 03 11;67(3):421-437. Epub 2019 Jan 11.

John Van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge, United Kingdom.

Schwann cells respond to nerve injury by cellular reprogramming that generates cells specialized for promoting regeneration and repair. These repair cells clear redundant myelin, attract macrophages, support survival of damaged neurons, encourage axonal growth, and guide axons back to their targets. There are interesting parallels between this response and that found in other tissues. Read More

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http://doi.wiley.com/10.1002/glia.23532
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http://dx.doi.org/10.1002/glia.23532DOI Listing
March 2019
5 Reads

Melanopsin for precise optogenetic activation of astrocyte-neuron networks.

Glia 2019 Jan 11. Epub 2019 Jan 11.

Department of Functional and Systems Neurobiology, Instituto Cajal, CSIC, Madrid, Spain.

Optogenetics has been widely expanded to enhance or suppress neuronal activity and it has been recently applied to glial cells. Here, we have used a new approach based on selective expression of melanopsin, a G-protein-coupled photopigment, in astrocytes to trigger Ca signaling. Using the genetically encoded Ca indicator GCaMP6f and two-photon imaging, we show that melanopsin is both competent to stimulate robust IP3-dependent Ca signals in astrocyte fine processes, and to evoke an ATP/Adenosine-dependent transient boost of hippocampal excitatory synaptic transmission. Read More

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http://doi.wiley.com/10.1002/glia.23580
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http://dx.doi.org/10.1002/glia.23580DOI Listing
January 2019
16 Reads
6.031 Impact Factor

Extracellular ATP and glutamate drive pyruvate production and energy demand to regulate mitochondrial respiration in astrocytes.

Glia 2019 Jan 9. Epub 2019 Jan 9.

Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Madrid, Spain.

Astrocytes respond to energetic demands by upregulating glycolysis, lactate production, and respiration. This study addresses the role of respiration and calcium regulation of respiration as part of the astrocyte response to the workloads caused by extracellular ATP and glutamate. Extracellular ATP (100 μM to 1 mM) causes a Ca -dependent workload and fall of the cytosolic ATP/ADP ratio which acutely increases astrocytes respiration. Read More

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http://dx.doi.org/10.1002/glia.23574DOI Listing
January 2019

A novel myelin protein zero transgenic zebrafish designed for rapid readout of in vivo myelination.

Glia 2019 Jan 9. Epub 2019 Jan 9.

Department of Cell and Developmental Biology, University of Colorado School of Medicine, Aurora, Colorado.

Demyelination occurs following many neurological insults, most notably in multiple sclerosis (MS). Therapeutics that promote remyelination could slow the neurological decline associated with chronic demyelination; however, in vivo testing of candidate small molecule drugs and signaling cascades known to impact myelination is expensive and labor intensive. Here, we describe the development of a novel zebrafish line which uses the putative promoter of Myelin Protein Zero (mpz), a major structural protein in myelin, to drive expression of Enhanced Green Fluorescent Protein (mEGFP) specifically in the processes and nascent internodes of myelinating glia. Read More

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http://dx.doi.org/10.1002/glia.23559DOI Listing
January 2019
2 Reads

The K -channel TASK1 affects Oligodendroglial differentiation but not myelin restoration.

Glia 2019 Jan 9. Epub 2019 Jan 9.

Department of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany.

In multiple sclerosis, demyelination occurs as a consequence of chronic autoimmunity in the central nervous system causing progressive neurological impairment in patients. After a demyelinating event, new myelin sheaths are formed by adult oligodendroglial progenitor cells; a process called remyelination. However, remyelination often fails in multiple sclerosis due to insufficient recruitment and differentiation of oligodendroglial precursor cells. Read More

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http://dx.doi.org/10.1002/glia.23577DOI Listing
January 2019

p75 regulates brain mononuclear cell function and neuronal structure in Toxoplasma infection-induced neuroinflammation.

Glia 2019 01;67(1):193-211

Otto-von-Guericke University Magdeburg, Institute of Inflammation and Neurodegeneration, Medical Faculty, Magdeburg, Germany.

Neurotrophins mediate neuronal growth, differentiation, and survival via tropomyosin receptor kinase (Trk) or p75 neurotrophin receptor (p75 ) signaling. The p75 is not exclusively expressed by neurons but also by certain immune cells, implying a role for neurotrophin signaling in the immune system. In this study, we investigated the effect of p75 on innate immune cell behavior and on neuronal morphology upon chronic Toxoplasma gondii (T. Read More

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http://dx.doi.org/10.1002/glia.23553DOI Listing
January 2019
1 Read
6.031 Impact Factor

CD11a expression distinguishes infiltrating myeloid cells from plaque-associated microglia in Alzheimer's disease.

Glia 2018 Dec 26. Epub 2018 Dec 26.

Sue and Bill Gross Stem Cell Research Center, University of California Irvine, Irvine, California.

Alzheimer's disease (AD) is the leading cause of age-related neurodegeneration and is characterized neuropathologically by the accumulation of insoluble beta-amyloid (Aβ) peptides. In AD brains, plaque-associated myeloid (PAM) cells cluster around Aβ plaques but fail to effectively clear Aβ by phagocytosis. PAM cells were originally thought to be brain-resident microglia. Read More

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http://dx.doi.org/10.1002/glia.23575DOI Listing
December 2018

Low sulfated heparins target multiple proteins for central nervous system repair.

Glia 2018 Dec 26. Epub 2018 Dec 26.

Institute of Infection, Immunity, and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK.

The lack of endogenous repair following spinal cord injury (SCI) accounts for the frequent permanent deficits for which effective treatments are absent. Previously, we demonstrated that low sulfated modified heparin mimetics (LS-mHeps) attenuate astrocytosis, suggesting they may represent a novel therapeutic approach. mHeps are glycomolecules with structural similarities to resident heparan sulfates (HS), which modulate cell signaling by both sequestering ligands, and acting as cofactors in the formation of ligand-receptor complexes. Read More

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http://doi.wiley.com/10.1002/glia.23562
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http://dx.doi.org/10.1002/glia.23562DOI Listing
December 2018
3 Reads

Stroke target identification guided by astrocyte transcriptome analysis.

Glia 2018 Dec 26. Epub 2018 Dec 26.

German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.

Astrocytes support normal brain function, but may also contribute to neurodegeneration when they become reactive under pathological conditions such as stroke. However, the molecular underpinnings of this context-dependent interplay between beneficial and detrimental properties in reactive astrogliosis have remained incompletely understood. Therefore, using the RiboTag technique, we immunopurified translating mRNAs specifically from astrocytes 72 hr after transient middle cerebral artery occlusion in mice (tMCAO), thereby generating a stroke-specific astroglial translatome database. Read More

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http://dx.doi.org/10.1002/glia.23544DOI Listing
December 2018

Necl-4/Cadm4 recruits Par-3 to the Schwann cell adaxonal membrane.

Glia 2018 Dec 26. Epub 2018 Dec 26.

Department of Neuroscience and Physiology, Neuroscience Institute, New York, New York.

Interactions between axons and Schwann cells are essential for the acquisition of Schwann cell radial and longitudinal polarity and myelin sheath assembly. In the internode, the largest of these longitudinal domains, axon-Schwann cell interactions are mediated by the Nectin-like (Necl) cell adhesion proteins, also known as SynCAMs or Cadms. In particular, Necl-1/Cadm3 expressed on the axon surface binds to Necl-4/Cadm4 expressed along the adaxonal membrane of myelinating Schwann cells. Read More

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http://doi.wiley.com/10.1002/glia.23578
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http://dx.doi.org/10.1002/glia.23578DOI Listing
December 2018
3 Reads

Regional and functional heterogeneity of antigen presenting cells in the mouse brain and meninges.

Glia 2018 Dec 26. Epub 2018 Dec 26.

Department of Anatomy and Developmental Biology, Monash Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.

The central nervous system (CNS) is considered to be immune privileged, owing in part to the absence of major histocompatibility (MHC) class II cells in the healthy brain parenchyma. However, systemic inflammation can activate microglia to express MHC class II, suggesting that systemic inflammation may be sufficient to mature microglia into functional antigen presenting cells (APCs). We examined the effects of systemic lipopolysaccharide (LPS)-induced inflammation on the phenotype and function of putative APCs within the mouse brain parenchyma, as well as its supporting tissues-the choroid plexus and meninges. Read More

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http://dx.doi.org/10.1002/glia.23581DOI Listing
December 2018
6.031 Impact Factor

Human immunodeficiency virus Type-1 single-stranded RNA activates the NLRP3 inflammasome and impairs autophagic clearance of damaged mitochondria in human microglia.

Glia 2018 Dec 24. Epub 2018 Dec 24.

Department of Pediatrics, Division of Infectious Diseases, University of California San Diego, La Jolla, California.

Despite the availability of antiretroviral therapy (ART) that fully suppresses human immunodeficiency virus type-1 (HIV), markers of inflammation and minor neurocognitive impairment are frequently identified in HIV-infected persons. Increasing data support that low-level replication defective viral RNA is made by infected cells despite the absence of infectious virus. Specific GU-rich single-stranded RNA from the HIV long terminal repeat region (ssRNA40) signaling through toll-like receptor (TLR)-7 and -8 has been shown to induce the secretion of interleukin-1β (IL-1β) in primary monocytes. Read More

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http://dx.doi.org/10.1002/glia.23568DOI Listing
December 2018

Spinal IL-36γ/IL-36R participates in the maintenance of chronic inflammatory pain through astroglial JNK pathway.

Glia 2019 03 21;67(3):438-451. Epub 2018 Dec 21.

Department of Central Laboratory, Shanghai Children's Hospital, Shanghai Jiaotong University, Shanghai, China.

Emerging evidence indicates that spinal neuroinflammation contributes to the maintenance of chronic inflammatory pain. IL-36, as a novel member of the interleukin (IL)-1 super-family cytokines, plays an important role in inflammatory responses. The present study aimed to investigate the role of spinal IL-36 and IL-36 receptor (IL-36R) signaling in the pathology of chronic inflammatory pain. Read More

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http://dx.doi.org/10.1002/glia.23552DOI Listing
March 2019
1 Read
6.031 Impact Factor

Interleukin-1beta released by microglia initiates the enhanced glutamatergic activity in the spinal dorsal horn during paclitaxel-associated acute pain syndrome.

Glia 2019 03 21;67(3):482-497. Epub 2018 Dec 21.

Department of Pharmaceutical and Biomedical Sciences, The University of Georgia College of Pharmacy, Athens, Georgia.

Patients receiving paclitaxel for cancer treatment often develop an acute pain syndrome (paclitaxel-associated acute pain syndrome, P-APS), which occurs immediately after paclitaxel treatment. Mechanisms underlying P-APS remain largely unknown. We recently reported that rodents receiving paclitaxel develop acute pain and activation of spinal microglial toll like receptor 4 (TLR4) by paclitaxel penetrating into the spinal cord is a critical event in the genesis of P-APS. Read More

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http://dx.doi.org/10.1002/glia.23557DOI Listing
March 2019
1 Read

Preclinical stress originates in the rat optic nerve head during development of autoimmune optic neuritis.

Glia 2019 03 21;67(3):512-524. Epub 2018 Dec 21.

Department of Neurology, University Clinic Heidelberg, Heidelberg, Germany.

Optic neuritis is a common manifestation of multiple sclerosis, an inflammatory demyelinating disease of the CNS. Although it is the presenting symptom in many cases, the initial events are currently unknown. However, in the earliest stages of autoimmune optic neuritis in rats, pathological changes are already apparent such as microglial activation and disturbances in myelin ultrastructure of the optic nerves. Read More

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http://doi.wiley.com/10.1002/glia.23560
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http://dx.doi.org/10.1002/glia.23560DOI Listing
March 2019
6 Reads

Morphological profile determines the frequency of spontaneous calcium events in astrocytic processes.

Glia 2019 02 22;67(2):246-262. Epub 2018 Nov 22.

Brain Science Institute (BSI), RIKEN, Wako-shi, Saitama, Japan.

Astrocytes express a complex repertoire of intracellular Ca transients (events) that represent a major form of signaling within individual cells and in astrocytic syncytium. These events have different spatiotemporal profiles, which are modulated by neuronal activity. Spontaneous Ca events appear more frequently in distal astrocytic processes and independently from each other. Read More

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http://dx.doi.org/10.1002/glia.23537DOI Listing
February 2019

Targeting microglia attenuates neuroinflammation-related neural damage in mice carrying human PLP1 mutations.

Glia 2019 02 22;67(2):277-290. Epub 2018 Nov 22.

Department of Neurology, Section of Developmental Neurobiology, University Hospital Wuerzburg, Wuerzburg, Germany.

Genetically caused neurological disorders of the central nervous system (CNS) usually result in poor or even fatal clinical outcome and few or no causative treatments are available. Often, these disorders are associated with disease-amplifying neuroinflammation, a feature shared by progressive forms of multiple sclerosis (PMS), another poorly treatable disorder of the CNS. We have previously generated two mouse lines carrying distinct mutations in the oligodendrocytic PLP1 gene that have initially been identified in patients fulfilling clinical criteria for multiple sclerosis (MS). Read More

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http://doi.wiley.com/10.1002/glia.23539
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http://dx.doi.org/10.1002/glia.23539DOI Listing
February 2019
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Neuroinflammation in the central nervous system: Symphony of glial cells.

Glia 2018 Dec 11. Epub 2018 Dec 11.

Institute of Neuroscience, State Key Laboratory of Neuroscience, CAS Center for Excellence in Brain Science and Intelligence Technology, Chinese Academy of Sciences, Shanghai, China.

Neuroinflammation in the central nervous system (CNS) is an important subject of neuroimmunological research. Emerging evidence suggests that neuroinflammation is a key player in various neurological disorders, including neurodegenerative diseases and CNS injury. Neuroinflammation is a complex and well-orchestrated process by various groups of glial cells in CNS and peripheral immune cells. Read More

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http://dx.doi.org/10.1002/glia.23571DOI Listing
December 2018
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Astrocyte-targeted IL-10 production decreases proliferation and induces a downregulation of activated microglia/macrophages after PPT.

Glia 2018 Dec 11. Epub 2018 Dec 11.

Department of Cell Biology, Physiology and Immunology, Institute of Neuroscience, Universitat Autònoma de Barcelona, Barcelona, Spain.

When central nervous system (CNS) homeostasis is altered, microglial cells become rapidly activated, proliferate and release a broad range of molecules. Among the plethora of molecules involved in the regulation of microglial activation, cytokines are considered crucial. Although production of interleukin-10 (IL-10) has been demonstrated after different types of CNS injuries and associated with protective functions, the specific role played by IL-10 modulating microglial cells remains unclear. Read More

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http://dx.doi.org/10.1002/glia.23573DOI Listing
December 2018

miR-223 promotes regenerative myeloid cell phenotype and function in the demyelinated central nervous system.

Glia 2018 Dec 11. Epub 2018 Dec 11.

Division of BioMedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, St. John's, Newfoundland, Canada.

In the injured central nervous system, myeloid cells, including macrophages and microglia, are key contributors to both myelin injury and repair. This immense plasticity emphasizes the need to further understand the precise molecular mechanisms that contribute to the dynamic regulation of myeloid cell polarization and function. Herein, we demonstrate that miR-223 is upregulated in multiple sclerosis (MS) patient monocytes and the alternatively-activated and tissue-regenerating M2-polarized human macrophages and microglia. Read More

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http://dx.doi.org/10.1002/glia.23576DOI Listing
December 2018

Astrocyte progenitor transplantation promotes regeneration of bulbospinal respiratory axons, recovery of diaphragm function, and a reduced macrophage response following cervical spinal cord injury.

Glia 2019 03 11;67(3):452-466. Epub 2018 Dec 11.

Department of Neuroscience, Vickie and Jack Farber Institute for Neuroscience, Sidney Kimmel Medical College at Thomas Jefferson University, Philadelphia, Pennsylvania.

Stem/progenitor cell transplantation delivery of astrocytes is a potentially powerful strategy for spinal cord injury (SCI). Axon extension into SCI lesions that occur spontaneously or in response to experimental manipulations is often observed along endogenous astrocyte "bridges," suggesting that augmenting this response via astrocyte lineage transplantation can enhance axon regrowth. Given the importance of respiratory dysfunction post-SCI, we transplanted glial-restricted precursors (GRPs)-a class of lineage-restricted astrocyte progenitors-into the C2 hemisection model and evaluated effects on diaphragm function and the growth response of descending rostral ventral respiratory group (rVRG) axons that innervate phrenic motor neurons (PhMNs). Read More

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http://dx.doi.org/10.1002/glia.23555DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6355351PMC

TREM2 triggers microglial density and age-related neuronal loss.

Glia 2019 03 11;67(3):539-550. Epub 2018 Dec 11.

Neural Regeneration, Institute of Reconstructive Neurobiology, University Hospital of Bonn, University of Bonn, Bonn, Germany.

The microglial triggering receptor expressed on myeloid cells 2 (TREM2) signals via the activatory membrane adaptor molecule TYROBP. Genetic variants or mutations of TREM2 or TYROBP have been linked to inflammatory neurodegenerative diseases associated with aging. The typical aging process goes along with microglial changes and mild neuronal loss, but the exact contribution of TREM2 is still unclear. Read More

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http://dx.doi.org/10.1002/glia.23563DOI Listing

Oxytocin receptor agonist reduces perinatal brain damage by targeting microglia.

Glia 2019 02 2;67(2):345-359. Epub 2018 Dec 2.

PROTECT, Inserm U1141, Université Paris Diderot, Paris, France.

Prematurity and fetal growth restriction (FGR) are frequent conditions associated with adverse neurocognitive outcomes. We have previously identified early deregulation of genes controlling neuroinflammation as a putative mechanism linking FGR and abnormal trajectory of the developing brain. While the oxytocin system was also found to be impaired following adverse perinatal events, its role in the modulation of neuroinflammation in the developing brain is still unknown. Read More

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http://doi.wiley.com/10.1002/glia.23546
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http://dx.doi.org/10.1002/glia.23546DOI Listing
February 2019
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Oncogenic dependence of glioma cells on kish/TMEM167A regulation of vesicular trafficking.

Glia 2019 02 2;67(2):404-417. Epub 2018 Dec 2.

Instituto Cajal, CSIC, Madrid, Spain.

Genetic lesions in glioblastoma (GB) include constitutive activation of PI3K and EGFR pathways to drive cellular proliferation and tumor malignancy. An RNAi genetic screen, performed in Drosophila melanogaster to discover new modulators of GB development, identified a member of the secretory pathway: kish/TMEM167A. Downregulation of kish/TMEM167A impaired fly and human glioma formation and growth, with no effect on normal glia. Read More

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http://dx.doi.org/10.1002/glia.23551DOI Listing
February 2019

Augmented astrocyte microdomain Ca dynamics and parenchymal arteriole tone in angiotensin II-infused hypertensive mice.

Glia 2019 03 2;67(3):551-565. Epub 2018 Dec 2.

Department of Physiology, Augusta University, Augusta, Georgia.

Hypertension is an important contributor to cognitive decline but the underlying mechanisms are unknown. Although much focus has been placed on the effect of hypertension on vascular function, less is understood of its effects on nonvascular cells. Because astrocytes and parenchymal arterioles (PA) form a functional unit (neurovascular unit), we tested the hypothesis that hypertension-induced changes in PA tone concomitantly increases astrocyte Ca . Read More

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http://doi.wiley.com/10.1002/glia.23564
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http://dx.doi.org/10.1002/glia.23564DOI Listing
March 2019
8 Reads

Amyloid precursor protein and amyloid precursor-like protein 2 have distinct roles in modulating myelination, demyelination, and remyelination of axons.

Glia 2019 03 2;67(3):525-538. Epub 2018 Dec 2.

Department of Pathology, The University of Melbourne, Melbourne, Victoria, Australia.

The identification of factors that regulate myelination provides important insight into the molecular mechanisms that coordinate nervous system development and myelin regeneration after injury. In this study, we investigated the role of amyloid precursor protein (APP) and its paralogue amyloid precursor-like protein 2 (APLP2) in myelination using APP and APLP2 knockout (KO) mice. Given that BACE1 regulates myelination and myelin sheath thickness in both the peripheral and central nervous systems, we sought to determine if APP and APLP2, as alternate BACE1 substrates, also modulate myelination, and therefore provide a better understanding of the events regulating axonal myelination. Read More

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http://dx.doi.org/10.1002/glia.23561DOI Listing
March 2019
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Cuprizone-induced graded oligodendrocyte vulnerability is regulated by the transcription factor DNA damage-inducible transcript 3.

Glia 2019 02 3;67(2):263-276. Epub 2018 Dec 3.

Faculty of Medicine, LMU Munich, Chair of Neuroanatomy, Institute of Anatomy, Munich, Germany.

Oligodendrocytes are integral to efficient neuronal signaling. Loss of myelinating oligodendrocytes is a central feature of many neurological diseases, including multiple sclerosis (MS). The results of neuropathological studies suggest that oligodendrocytes react with differing sensitivity to toxic insults, with some cells dying early during lesion development and some cells being resistant for weeks. Read More

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http://doi.wiley.com/10.1002/glia.23538
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http://dx.doi.org/10.1002/glia.23538DOI Listing
February 2019
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Activated T cells induce proliferation of oligodendrocyte progenitor cells via release of vascular endothelial cell growth factor-A.

Glia 2018 11;66(11):2503-2513

Translational Neuroscience Center, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland.

Neuroinflammatory diseases such as multiple sclerosis are characterized by infiltration of lymphocytes into the central nervous system followed by demyelination and axonal degeneration. While evidence suggests that activated T lymphocytes induce neurotoxicity and impair function of neural stem cells, the effect of T cells on oligodendrocyte progenitor cells (OPCs) is still uncertain, partly due to the difficulty in obtaining human OPCs. Here we studied the effect of activated T cells on OPCs using OPCs derived from human hematopoietic stem cells or from human fetal brain. Read More

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http://dx.doi.org/10.1002/glia.23501DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6278606PMC
November 2018

Inhibition of astrocyte FAK-JNK signaling promotes subventricular zone neurogenesis through CNTF.

Glia 2018 11;66(11):2456-2469

Department of Biomedical Sciences, Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee.

Astrocyte-derived ciliary neurotrophic factor (CNTF) promotes adult subventricular zone (SVZ) neurogenesis. We found that focal adhesion kinase (FAK) and JNK, but not ERK or P38, repress CNTF in vitro. Here, we defined the FAK-JNK pathway and its regulation of CNTF in mice, and the related leukemia inhibitory factor (LIF) and interleukin-6 (IL-6), which promote stem cell renewal at the expense of neurogenesis. Read More

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http://dx.doi.org/10.1002/glia.23498DOI Listing
November 2018