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https://www.readbyqxmd.com/read/28940767/human-mesenchymal-factors-induce-rat-hippocampal-and-human-neural-stem-cell-dependent-oligodendrogenesis
#1
Janusz J Jadasz, Lena Tepe, Felix Beyer, Iria Samper Agrelo, Rainer Akkermann, Lucas-Sebastian Spitzhorn, Maria Elena Silva, Richard O C Oreffo, Hans-Peter Hartung, Alessandro Prigione, Francisco J Rivera, James Adjaye, Patrick Küry
The generation of new oligodendrocytes is essential for adult brain repair in diseases such as multiple sclerosis. We previously identified the multifunctional p57kip2 protein as a negative regulator of myelinating glial cell differentiation and as an intrinsic switch of glial fate decision in adult neural stem cells (aNSCs). In oligodendroglial precursor cells (OPCs), p57kip2 protein nuclear exclusion was recently found to be rate limiting for differentiation to proceed. Furthermore, stimulation with mesenchymal stem cell (MSC)-derived factors enhanced oligodendrogenesis by yet unknown mechanisms...
September 22, 2017: Glia
https://www.readbyqxmd.com/read/28940645/lineage-tracing-reveals-dynamic-changes-in-oligodendrocyte-precursor-cells-following-cuprizone-induced-demyelination
#2
Emily G Baxi, Joseph DeBruin, Jing Jin, Hayley J Strasburger, Matthew D Smith, Jennifer L Orthmann-Murphy, Jason T Schott, Amanda N Fairchild, Dwight E Bergles, Peter A Calabresi
The regeneration of oligodendrocytes is a crucial step in recovery from demyelination, as surviving oligodendrocytes exhibit limited structural plasticity and rarely form additional myelin sheaths. New oligodendrocytes arise through the differentiation of platelet-derived growth factor receptor α (PDGFRα) expressing oligodendrocyte progenitor cells (OPCs) that are widely distributed throughout the CNS. Although there has been detailed investigation of the behavior of these progenitors in white matter, recent studies suggest that disease burden in multiple sclerosis (MS) is more strongly correlated with gray matter atrophy...
September 22, 2017: Glia
https://www.readbyqxmd.com/read/28940651/mechanical-plasticity-during-oligodendrocyte-differentiation-and-myelination
#3
REVIEW
Helena S Domingues, Andrea Cruz, Jonah R Chan, João B Relvas, Boris Rubinstein, Inês Mendes Pinto
In the central nervous system, oligodendrocyte precursor cells are exclusive in their potential to differentiate into myelinating oligodendrocytes. Oligodendrocyte precursor cells migrate within the parenchyma and extend cell membrane protrusions that ultimately evolve into myelinating sheaths able to wrap neuronal axons and significantly increase their electrical conductivity. The subcellular force generating mechanisms driving morphological and functional transformations during oligodendrocyte differentiation and myelination remain elusive...
September 21, 2017: Glia
https://www.readbyqxmd.com/read/28925578/combined-fetal-inflammation-and-postnatal-hypoxia-causes-myelin-deficits-and-autism-like-behavior-in-a-rat-model-of-diffuse-white-matter-injury
#4
Erik van Tilborg, E J Marijke Achterberg, Caren M van Kammen, Annette van der Toorn, Floris Groenendaal, Rick M Dijkhuizen, Cobi J Heijnen, Louk J M J Vanderschuren, Manon N J L Benders, Cora H A Nijboer
Diffuse white matter injury (WMI) is a serious problem in extremely preterm infants, and is associated with adverse neurodevelopmental outcome, including cognitive impairments and an increased risk of autism-spectrum disorders. Important risk factors include fetal or perinatal inflammatory insults and fluctuating cerebral oxygenation. However, the exact mechanisms underlying diffuse WMI are not fully understood and no treatment options are currently available. The use of clinically relevant animal models is crucial to advance knowledge on the pathophysiology of diffuse WMI, allowing the definition of novel therapeutic targets...
September 19, 2017: Glia
https://www.readbyqxmd.com/read/28925561/nestin-expressing-cell-types-in-the-temporal-lobe-and-hippocampus-morphology-differentiation-and-proliferative-capacity
#5
Joan Liu, Cheryl Reeves, Thomas Jacques, Andrew McEvoy, Anna Miserocchi, Pamela Thompson, Sanjay Sisodiya, Maria Thom
Nestin is expressed in immature neuroepithelial and progenitor cell types and transiently upregulated in proliferative neuroglial cells responding to acute brain injury, including following seizures. In 36 temporal lobe (TLobe) specimens from patients with TLobe epilepsy (age range 8-60 years) we studied the number, distribution and morphology of nestin-expressing cells (NEC) in the pes, hippocampus body, parahippocampal gyrus, amygdala, temporal cortex and pole compared with post mortem control tissues from 26 cases (age range 12 gestational weeks to 76 years)...
September 19, 2017: Glia
https://www.readbyqxmd.com/read/28925083/selective-knockout-of-astrocytic-na-h-exchanger-isoform-1-reduces-astrogliosis-bbb-damage-infarction-and-improves-neurological-function-after-ischemic-stroke
#6
Gulnaz Begum, Shanshan Song, Shaoxia Wang, Hanshu Zhao, Mohammad Iqbal H Bhuiyan, Eric Li, Rachel Nepomuceno, Qing Ye, Ming Sun, Michael Joseph Calderon, Donna B Stolz, Claudette St Croix, Simon C Watkins, Yinhuai Chen, Pingnian He, Gary E Shull, Dandan Sun
Stimulation of Na(+) /H(+) exchanger isoform 1 (NHE1) in astrocytes causes ionic dysregulation under ischemic conditions. In this study, we created a Nhe1(flox/flox) (Nhe1(f/f) ) mouse line with exon 5 of Nhe1 flanked with two loxP sites and selective ablation of Nhe1 in astrocytes was achieved by crossing Nhe1(f/f) mice with Gfap-Cre(ERT2) Cre-recombinase mice. Gfap-Cre(ERT2+/-) ;Nhe1(f/f) mice at postnatal day 60-90 were treated with either corn oil or tamoxifen (Tam, 75 mg/kg/day, i.p.) for 5 days. After 30 days post-injection, mice underwent transient middle cerebral artery occlusion (tMCAO) to induce ischemic stroke...
September 19, 2017: Glia
https://www.readbyqxmd.com/read/28925029/loss-of-gas6-and-axl-signaling-results-in-extensive-axonal-damage-motor-deficits-prolonged-neuroinflammation-and-less-remyelination-following-cuprizone-exposure
#7
Alex K Ray, Juwen C DuBois, Ross C Gruber, Hillary M Guzik, Maria E Gulinello, Geoffrey Perumal, Cedric Raine, Lauren Kozakiewicz, Julie Williamson, Bridget Shafit-Zagardo
The TAM (Tyro3, Axl, and MerTK) family of receptor tyrosine kinases (RTKs) and their ligands, Gas6 and ProS1, are important for innate immune responses and central nervous system (CNS) homeostasis. While only Gas6 directly activates Axl, ProS1 activation of Tyro3/MerTK can indirectly activate Axl through receptor heterodimerization. Therefore, we generated Gas6(-/-) Axl(-/-) double knockout (DKO) mice to specifically examine the contribution of this signaling axis while retaining ProS1 signaling through Tyro3 and MerTK...
September 19, 2017: Glia
https://www.readbyqxmd.com/read/28921694/protease-activated-receptor-2-controls-myelin-development-resiliency-and-repair
#8
Hyesook Yoon, Maja Radulovic, Grant Walters, Alex R Paulsen, Kristen Drucker, Phillip Starski, Jianmin Wu, David P Fairlie, Isobel A Scarisbrick
Oligodendrocytes are essential regulators of axonal energy homeostasis and electrical conduction and emerging target cells for restoration of neurological function. Here we investigate the role of protease activated receptor 2 (PAR2), a unique protease activated G protein-coupled receptor, in myelin development and repair using the spinal cord as a model. Results demonstrate that genetic deletion of PAR2 accelerates myelin production, including higher proteolipid protein (PLP) levels in the spinal cord at birth and higher levels of myelin basic protein and thickened myelin sheaths in adulthood...
September 18, 2017: Glia
https://www.readbyqxmd.com/read/28906039/novel-role-of-the-nociceptin-system-as-a-regulator-of-glutamate-transporter-expression-in-developing-astrocytes
#9
Logan C Meyer, Caitlin E Paisley, Esraa Mohamed, John W Bigbee, Tomasz Kordula, Hope Richard, Kabirullah Lutfy, Carmen Sato-Bigbee
Our previous results showed that oligodendrocyte development is regulated by both nociceptin and its G-protein coupled receptor, the nociceptin/orphanin FQ receptor (NOR). The present in vitro and in vivo findings show that nociceptin plays a crucial conserved role regulating the levels of the glutamate/aspartate transporter GLAST/EAAT1 in both human and rodent brain astrocytes. This nociceptin-mediated response takes place during a critical developmental window that coincides with the early stages of astrocyte maturation...
September 14, 2017: Glia
https://www.readbyqxmd.com/read/28906027/sur1-trpm4-and-aqp4-form-a-heteromultimeric-complex-that-amplifies-ion-water-osmotic-coupling-and-drives-astrocyte-swelling
#10
Jesse A Stokum, Min S Kwon, Seung K Woo, Orest Tsymbalyuk, Rudi Vennekens, Volodymyr Gerzanich, J Marc Simard
Astrocyte swelling occurs after central nervous system injury and contributes to brain swelling, which can increase mortality. Mechanisms proffered to explain astrocyte swelling emphasize the importance of either aquaporin-4 (AQP4), an astrocyte water channel, or of Na(+) -permeable channels, which mediate cellular osmolyte influx. However, the spatio-temporal functional interactions between AQP4 and Na(+) -permeable channels that drive swelling are poorly understood. We hypothesized that astrocyte swelling after injury is linked to an interaction between AQP4 and Na(+) -permeable channels that are newly upregulated...
September 14, 2017: Glia
https://www.readbyqxmd.com/read/28887860/regulation-of-radial-glial-process-growth-by-glutamate-via-mglur5-trpc3-and-neuregulin-erbb4
#11
Lauri M Louhivuori, Pauli M Turunen, Verna Louhivuori, Venkatram Yellapragada, Tommy Nordström, Per Uhlén, Karl E Åkerman
Radial glial cells play an essential role through their function as guides for neuronal migration during development. Disruption of metabotropic glutamate receptor 5 (mGluR5) function retards the growth of radial glial processes in vitro. Neuregulins (NRG) are activated by proteolytic cleavage and regulate (radial) glial maintenance via ErbB3/ErbB4 receptors. We show here that blocking ErbB4 disrupts radial process extension. Soluble NRG acting on ErbB4 receptors is able to promote radial process extension in particular where process elongation has been impeded by blockade of mGluR5, the nonselective cation channel canonical transient receptor potential 3 (TRPC3), or matrix metalloproteases (MMP)...
September 9, 2017: Glia
https://www.readbyqxmd.com/read/28885722/astrocytic-signaling-supports-hippocampal-prefrontal-theta-synchronization-and-cognitive-function
#12
Vanessa Morais Sardinha, Sónia Guerra-Gomes, Inês Caetano, Gabriela Tavares, Manuella Martins, Joana Santos Reis, Joana Sofia Correia, Andreia Teixeira-Castro, Luísa Pinto, Nuno Sousa, João Filipe Oliveira
Astrocytes interact with neurons at the cellular level through modulation of synaptic formation, maturation, and function, but the impact of such interaction into behavior remains unclear. Here, we studied the dominant negative SNARE (dnSNARE) mouse model to dissect the role of astrocyte-derived signaling in corticolimbic circuits, with implications for cognitive processing. We found that the blockade of gliotransmitter release in astrocytes triggers a critical desynchronization of neural theta oscillations between dorsal hippocampus and prefrontal cortex...
September 8, 2017: Glia
https://www.readbyqxmd.com/read/28856805/reactive-astrocyte-cox2-pge2-production-inhibits-oligodendrocyte-maturation-in-neonatal-white-matter-injury
#13
Lawrence R Shiow, Geraldine Favrais, Lucas Schirmer, Anne-Laure Schang, Sara Cipriani, Christian Andres, Jaclyn N Wright, Hiroko Nobuta, Bobbi Fleiss, Pierre Gressens, David H Rowitch
Inflammation is a major risk factor for neonatal white matter injury (NWMI), which is associated with later development of cerebral palsy. Although recent studies have demonstrated maturation arrest of oligodendrocyte progenitor cells (OPCs) in NWMI, the identity of inflammatory mediators with direct effects on OPCs has been unclear. Here, we investigated downstream effects of pro-inflammatory IL-1β to induce cyclooxygenase-2 (COX2) and prostaglandin E2 (PGE2) production in white matter. First, we assessed COX2 expression in human fetal brain and term neonatal brain affected by hypoxic-ischemic encephalopathy (HIE)...
August 30, 2017: Glia
https://www.readbyqxmd.com/read/28856727/cholesterol-regulates-polymodal-sensory-transduction-in-m%C3%A3-ller-glia
#14
Monika Lakk, Oleg Yarishkin, Jackson M Baumann, Anthony Iuso, David Križaj
Over- and underexposure to cholesterol activates glia in neurodegenerative brain and retinal diseases but the molecular targets of cholesterol in glial cells are not known. Here, we report that disruption of unesterified membrane cholesterol content modulates the transduction of chemical, mechanical and temperature stimuli in mouse Müller cells. Activation of TRPV4 (transient receptor potential vanilloid type 4), a nonselective polymodal cation channel was studied following the removal or supplementation of cholesterol using the methyl-beta cyclodextrin (MβCD) delivery vehicle...
August 30, 2017: Glia
https://www.readbyqxmd.com/read/28856719/oligodendrocyte-rasg12v-expressed-in-its-endogenous-locus-disrupts-myelin-structure-through-increased-mapk-nitric-oxide-and-notch-signaling
#15
Haley E Titus, Alejandro López-Juárez, Sadiq H Silbak, Tilat A Rizvi, Madeleine Bogard, Nancy Ratner
Costello syndrome (CS) is a gain of function Rasopathy caused by heterozygous activating mutations in the HRAS gene. Patients show brain dysfunction that can include abnormal brain white matter. Transgenic activation of HRas in the entire mouse oligodendrocyte lineage resulted in myelin defects and behavioral abnormalities, suggesting roles for disrupted myelin in CS brain dysfunction. Here, we studied a mouse model in which the endogenous HRas gene is conditionally replaced by mutant HRasG12V in mature oligodendrocytes, to separate effects in mature myelinating cells from developmental events...
August 30, 2017: Glia
https://www.readbyqxmd.com/read/28850719/complement-3a-receptor-in-dorsal-horn-microglia-mediates-pronociceptive-neuropeptide-signaling
#16
Suzanne Doolen, Jennifer Cook, Maureen Riedl, Kelley Kitto, Shinichi Kohsaka, Christopher N Honda, Carolyn A Fairbanks, Bradley K Taylor, Lucy Vulchanova
The complement 3a receptor (C3aR1) participates in microglial signaling under pathological conditions and was recently shown to be activated by the neuropeptide TLQP-21. We previously demonstrated that TLQP-21 elicits hyperalgesia and contributes to nerve injury-induced hypersensitivity through an unknown mechanism in the spinal cord. Here we determined that this mechanism requires C3aR1 and that microglia are the cellular target for TLQP-21. We propose a novel neuroimmune signaling pathway involving TLQP-21-induced activation of microglial C3aR1 that then contributes to spinal neuroplasticity and neuropathic pain...
August 29, 2017: Glia
https://www.readbyqxmd.com/read/28850711/adamts-4-in-oligodendrocytes-contributes-to-myelination-with-an-impact-on-motor-function
#17
Mathilde Pruvost, Matthieu Lépine, Camille Leonetti, Olivier Etard, Mikaël Naveau, Véronique Agin, Fabian Docagne, Eric Maubert, Carine Ali, Evelyne Emery, Denis Vivien
Myelination is a late developmental process regulated by a set of inhibitory and stimulatory factors, including extracellular matrix components. Accordingly, chondroitin sulfate proteoglycans (CSPGs) act as negative regulators of myelination processes. A disintegrin and metalloproteinase with thrombospondin motifs type 4 (ADAMTS-4) is an extracellular protease capable of degrading CSPGs. Although exogenous ADAMTS-4 has been proven to be beneficial in several models of central nervous system (CNS) injuries, the physiological functions of endogenous ADAMTS-4 remain poorly understood...
August 29, 2017: Glia
https://www.readbyqxmd.com/read/28836393/the-microglial-fractalkine-receptor-is-not-required-for-activity-dependent-plasticity-in-the-mouse-visual-system
#18
Rebecca L Lowery, Marie-Eve Tremblay, Brittany E Hopkins, Ania K Majewska
Microglia have recently been implicated as key regulators of activity-dependent plasticity, where they contribute to the removal of inappropriate or excess synapses. However, the molecular mechanisms that mediate this microglial function are still not well understood. Although multiple studies have implicated fractalkine signaling as a mediator of microglia-neuron communications during synaptic plasticity, it is unclear whether this is a universal signaling mechanism or whether its role is limited to specific brain regions and stages of the lifespan...
August 24, 2017: Glia
https://www.readbyqxmd.com/read/28836308/siglec-h-is-a-microglia-specific-marker-that-discriminates-microglia-from-cns-associated-macrophages-and-cns-infiltrating-monocytes
#19
Hiroyuki Konishi, Masaaki Kobayashi, Taikan Kunisawa, Kenta Imai, Akira Sayo, Bernard Malissen, Paul R Crocker, Katsuaki Sato, Hiroshi Kiyama
Several types of myeloid cell are resident in the CNS. In the steady state, microglia are present in the CNS parenchyma, whereas macrophages reside in boundary regions of the CNS, such as perivascular spaces, the meninges and choroid plexus. In addition, monocytes infiltrate into the CNS parenchyma from circulation upon blood-brain barrier breakdown after CNS injury and inflammation. Although several markers, such as CD11b and ionized calcium-binding adapter molecule 1 (Iba1), are frequently used as microglial markers, they are also expressed by other types of myeloid cell and microglia-specific markers were not defined until recently...
August 24, 2017: Glia
https://www.readbyqxmd.com/read/28836307/genetic-dissection-of-oligodendroglial-and-neuronal-plp1-function-in-a-novel-mouse-model-of-spastic-paraplegia-type-2
#20
Katja A Lüders, Julia Patzig, Mikael Simons, Klaus-Armin Nave, Hauke B Werner
Proteolipid protein (PLP) is the most abundant integral membrane protein in compact central nervous system myelin, and null mutations of the PLP1 gene cause spastic paraplegia type 2 (SPG2). SPG2 patients and PLP-deficient mice exhibit only moderate abnormalities of myelin but progressive degeneration of long axons. Since Plp1 gene products are detected in a subset of neurons it has been suggested that the loss of neuronal Plp1 expression could be the cause of the axonal pathology. To test this hypothesis, we created mice with a floxed Plp1 allele for selective Cre-mediated recombination in neurons...
August 24, 2017: Glia
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