Academic literature on the topic 'Oligodendrocytes maturation'
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Journal articles on the topic "Oligodendrocytes maturation"
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Facchinetti, Roberta, Marta Valenza, Chiara Gomiero, Giulia Federica Mancini, Luca Steardo, Patrizia Campolongo, and Caterina Scuderi. "Co-Ultramicronized Palmitoylethanolamide/Luteolin Restores Oligodendrocyte Homeostasis via Peroxisome Proliferator-Activated Receptor-α in an In Vitro Model of Alzheimer’s Disease." Biomedicines 10, no. 6 (May 26, 2022): 1236. http://dx.doi.org/10.3390/biomedicines10061236.
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Oligodendrocytes are cells fundamental for brain functions as they form the myelin sheath and feed axons. They perform these critical functions thanks to the cooperation with other glial cells, mainly astrocytes. The astrocyte/oligodendrocyte crosstalk needs numerous mediators and receptors, such as peroxisome proliferator-activated receptors (PPARs). PPAR agonists promote oligodendrocyte precursor cells (OPCs) maturation in myelinating oligodendrocytes. In the Alzheimer’s disease brain, deposition of beta-amyloid (Aβ) has been linked to several alterations, including astrogliosis and changes in OPCs maturation. However, very little is known about the molecular mechanisms. Here, we investigated for the first time the maturation of OPCs co-cultured with astrocytes in an in vitro model of Aβ1–42 toxicity. We also tested the potential beneficial effect of the anti-inflammatory and neuroprotective composite palmitoylethanolamide and luteolin (co-ultra PEALut), which is known to engage the isoform alfa of the PPARs. Our results show that Aβ1–42 triggers astrocyte reactivity and inflammation and reduces the levels of growth factors important for OPCs maturation. Oligodendrocytes indeed show low cell surface area and few arborizations. Co-ultra PEALut counteracts the Aβ1–42-induced inflammation and astrocyte reactivity preserving the morphology of co-cultured oligodendrocytes through a mechanism that in some cases involves PPAR-α. This is the first evidence of the negative effects exerted by Aβ1–42 on astrocyte/oligodendrocyte crosstalk and discloses a never-explored co-ultra PEALut ability in restoring oligodendrocyte homeostasis.
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Seil, Fredrick J. "Tissue Culture Models of Myelination After Oligodendrocyte Transplantation." Journal of Neural Transplantation 1, no. 2 (1989): 49–55. http://dx.doi.org/10.1155/np.1989.49.
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Studies of myelination after transplantation of mature oligodendrocytes to cerebellar cultures in which oligodendrocyte maturation and myelination had been irreversibly inhibited by exposure to cytosine arabinoside were reviewed. Transplanted oligodendrocytes were derived from three sources, including cerebellar explants treated with kainic acid, dissociated oligodendrocyte cultures, and optic nerve fragments. Oligodendrocytes from all sources migrated into the host explants and myelinated appropriate axons. The time of appearance of myelin and the percentage of host cultures myelinated differed for the three sources of oligodendrocytes, however. Myelin was visible earliest and in the highest percentage of host explants transplanted with cultured dissociated oligodendrocytes, which were presumably the most free to migrate into the host tissue, and latest and in the lowest percentage of host cultures transplanted with optic nerve, from which oligodendrocytes were presumably least free to migrate. Some myelin-like membranes unassociated with axons appeared in cerebellar cultures transplanted with cultured dissociated oligodendrocytes, and not in cerebellar explants transplanted with oligodendrocytes from other sources. The formation of such myelin-like membranes was interpreted as a manifestation of oligodendrocyte hyperreactivity induced by culture in isolation.
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Nadon, N. L., I. D. Duncan, and L. D. Hudson. "A point mutation in the proteolipid protein gene of the ‘shaking pup’ interrupts oligodendrocyte development." Development 110, no. 2 (October 1, 1990): 529–37. http://dx.doi.org/10.1242/dev.110.2.529.
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The differentiation of the oligodendrocyte from its bipotential progenitor culminates in the production of the myelin-specific proteins and the elaboration of membrane processes that ensheath the axon. Mutations in proteolipid protein (PLP) and its alternatively spliced isoform DM-20, the major protein constituents of central nervous system myelin, are characterized by a significant reduction in the number of mature oligodendrocytes, resulting in severe hypomyelination, tremor and early death. The canine shaking pup carries such a mutation, a single base change that substitutes a proline for a histidine near the first transmembrane region of PLP and DM-20. This mutation hinders oligodendrocyte differentiation, as evidence by a splicing pattern at the PLP locus characteristic of immature oligodendrocytes. The spliced transcript expressed earliest in development, DM-20, continues to be overexpressed in shaking pup oligodendrocytes. The disruption of the normal maturation schedule in these X-linked dysmyelinating disorders suggests that PLP or DM-20 plays a fundamental role in oligodendrocyte development. We propose that, while the more abundant PLP is the primary structural component of myelin, DM-20 may be critical to oligodendrocyte maturation.
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Louis, JC, E. Magal, S. Takayama, and S. Varon. "CNTF protection of oligodendrocytes against natural and tumor necrosis factor-induced death." Science 259, no. 5095 (January 29, 1993): 689–92. http://dx.doi.org/10.1126/science.8430320.
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A proportion of developing oligodendrocytes undergo natural cell death by apoptosis, and mature oligodendrocytes die, either by apoptosis or necrosis, in response to injurious signals such as cytotoxic cytokines and complement. Ciliary neurotrophic factor (CNTF), a trophic factor found in astrocytes in the central nervous system (CNS), promoted the survival and maturation of cultured oligodendrocytes. This trophic factor also protected oligodendrocytes from death induced by tumor necrosis factors (apoptosis) but not against complement (necrosis). These results suggest that CNTF functions in the survival of oligodendrocytes during development and may lead to therapeutic approaches for degenerative diseases of the CNS that involve oligodendrocyte destruction.
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Ono, K., R. Bansal, J. Payne, U. Rutishauser, and R. H. Miller. "Early development and dispersal of oligodendrocyte precursors in the embryonic chick spinal cord." Development 121, no. 6 (June 1, 1995): 1743–54. http://dx.doi.org/10.1242/dev.121.6.1743.
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Oligodendrocytes, the myelinating cells of the vertebrate CNS, originally develop from cells of the neuroepithelium. Recent studies suggest that spinal cord oligodendrocyte precursors are initially localized in the region of the ventral ventricular zone and subsequently disperse throughout the spinal cord. The characteristics of these early oligodendrocyte precursors and their subsequent migration has been difficult to assay directly in the rodent spinal cord due to a lack of appropriate reagents. In the developing chick spinal cord, we show that oligodendrocyte precursors can be specifically identified by labeling with O4 monoclonal antibody. In contrast to rodent oligodendrocyte precursors, which express O4 immunoreactivity only during the later stages of maturation, in the chick O4 immunoreactivity appears very early and its expression is retained through cellular maturation. In embryos older than stage 35, O4+ cells represent the most immature, self-renewing, cells of the chick spinal cord oligodendrocyte lineage. In the intact chick spinal cord, the earliest O4+ cells are located at the ventral ventricular zone where they actually contribute to the ventricular lining of the central canal. The subsequent migration of O4+ cells into the dorsal region of the spinal cord temporally correlates with the capacity of isolated dorsal spinal cord to generate oligodendrocytes in vitro. Biochemical analysis suggests O4 labels a POA-like antigen on the surface of chick spinal cord oligodendrocyte precursors. These studies provide direct evidence for the ventral ventricular origin of spinal cord oligodendrocytes, and suggest that this focal source of oligodendrocytes is a general characteristic of vertebrate development.
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Mariyath, Mubeena P. M., Mehdi H. Shahi, Shirin Farheen, Mohd Tayyab, Nabeela Khanam, and Asif Ali. "Novel Homeodomain Transcription Factor Nkx2.2 in the Brain Tumor Development." Current Cancer Drug Targets 20, no. 5 (June 5, 2020): 335–40. http://dx.doi.org/10.2174/1568009618666180102111539.
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Background: Complex central nervous system (CNS) is made up of neuronal cells and glial cells. Cells of central nervous system are able to regenerate after injury and during repairing. Sonic hedgehog pathway initiated by Shh-N a glycoprotein plays vital role in CNS patterning growth, development and now tumorigenesis. Nkx2.2 homeodomain transcription factor is an effecter molecule, which is positively regulated by Shh during normal growth. Nkx2.2 is essential for V3 domain specification during neural tube patterning at embryonic stage. MBP + oligodendrocytes are differentiated from progenitor cells which express Olig2. Nx2.2 is co-expressed with Olig2 in oligodendrocytes and is essential for later stage of oligodendrocyte maturation. Objective: This review paper explores the potential role of Nkx2.2 transcription factor in glioblastoma development. Conclusion: Shh pathway plays a vital role in oligodendrocytes differentiation and Nkx2.2 transcription factor is essential for oligodendrocytes differentiation and maturation. Intriguingly, down regulation of Nkx2.2 transcription factor with aberrant Shh signaling pathway is reported in glioma samples. So here it is suggested that Nkx2.2 expression pattern could be used as a potential biomarker for the early diagnosis of glioma.
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Vostrikov, Victor, and Natalya Uranova. "Age-Related Increase in the Number of Oligodendrocytes Is Dysregulated in Schizophrenia and Mood Disorders." Schizophrenia Research and Treatment 2011 (2011): 1–10. http://dx.doi.org/10.1155/2011/174689.
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The postnatal maturation of the human prefrontal cortex is associated with substantial increase of number of oligodendrocytes. Previously, we reported decreased numerical density of oligodendrocytes in the prefrontal cortex in schizophrenia and mood disorders. To gain further understanding of the role oligodendrocytes in pathogenesis of schizophrenia and mood disorders, we examined the effect of the age on the number of oligodendrocytes in the prefrontal cortex in schizophrenia, bipolar disorder, and major depressive disorder. We revealed the age-related increase in numerical density of oligodendrocytes in layer VI and adjacent white matter of BA10 and BA 9 in normal controls but not in schizophrenia, bipolar disorder, and major depressive disorder. The absence of normal increase in the number of oligodendrocytes in gray and white matter with age in schizophrenia and mood disorders suggests that age-related process of oligodendrocyte increase is dysregulated in schizophrenia and mood disorders.
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Aberle, Tim, Sandra Piefke, Simone Hillgärtner, Ernst R. Tamm, Michael Wegner, and Melanie Küspert. "Transcription factor Zfp276 drives oligodendroglial differentiation and myelination by switching off the progenitor cell program." Nucleic Acids Research 50, no. 4 (February 7, 2022): 1951–68. http://dx.doi.org/10.1093/nar/gkac042.
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Abstract In oligodendrocytes of the vertebrate central nervous system a complex network of transcriptional regulators is required to ensure correct and timely myelination of neuronal axons. Here we identify Zfp276, the only mammalian ZAD-domain containing zinc finger protein, as a transcriptional regulator of oligodendrocyte differentiation and central myelination downstream of Sox10. In the central nervous system, Zfp276 is exclusively expressed in mature oligodendrocytes. Oligodendroglial deletion of Zfp276 led to strongly reduced expression of myelin genes in the early postnatal mouse spinal cord. Retroviral overexpression of Zfp276 in cultured oligodendrocyte precursor cells induced precocious expression of maturation markers and myelin genes, further supporting its role in oligodendroglial differentiation. On the molecular level, Zfp276 directly binds to and represses Sox10-dependent gene regulatory regions of immaturity factors and functionally interacts with the transcriptional repressor Zeb2 to enable fast transition of oligodendrocytes to the myelinating stage.
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Rosko, Lauren, Victoria N. Smith, Reiji Yamazaki, and Jeffrey K. Huang. "Oligodendrocyte Bioenergetics in Health and Disease." Neuroscientist 25, no. 4 (August 20, 2018): 334–43. http://dx.doi.org/10.1177/1073858418793077.
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The human brain weighs approximately 2% of the body; however, it consumes about 20% of a person’s total energy intake. Cellular bioenergetics in the central nervous system involves a delicate balance between biochemical processes engaged in energy conversion and those responsible for respiration. Neurons have high energy demands, which rely on metabolic coupling with glia, such as with oligodendrocytes and astrocytes. It has been well established that astrocytes recycle and transport glutamine to neurons to make the essential neurotransmitters, glutamate and GABA, as well as shuttle lactate to support energy synthesis in neurons. However, the metabolic role of oligodendrocytes in the central nervous system is less clear. In this review, we discuss the energetic demands of oligodendrocytes in their survival and maturation, the impact of altered oligodendrocyte energetics on disease pathology, and the role of energetic metabolites, taurine, creatine, N-acetylaspartate, and biotin, in regulating oligodendrocyte function.
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Ferraresi, S., I. Lorenzetti, R. Nemni, J. Kamholz, ML Feltri, and L. Wrabetz. "Toward a transgenic mouse model of remyelination." Multiple Sclerosis Journal 3, no. 2 (April 1997): 80–83. http://dx.doi.org/10.1177/135245859700300204.
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The molecular mechanisms necessary for remyelination by oligodendrocytes remain unexplored. We previously characterized a myelin basic protein promoter-lacZ (MBP-lacZ) transgene whose expression is regulated uniquely during development, and also in pathological situations, suggesting that it may be a useful reporter of molecular mechanisms during remyelination. As a first step toward creating a transgenic mouse model of remyelination, we cultured oligodendrocytes from these transgenic mice and showed that expression of MBP-lacZ appeared in parallel with a marker of oligodendrocyte maturation, galactocerebroside (GC). In addition, basic fibroblast growth factor blocked the expression of both MBP-lacZ and GC in these cells. Therefore, expression of MBP-lacZ reflects not only the developmental stage of oligodendrocytes, but also extrinsic influences on oligodendrocytes. These data suggest that MBP-lacZ may be a useful marker in transgenic mouse models of remyelination.
Dissertations / Theses on the topic "Oligodendrocytes maturation"
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Ford, Catriona Barbara. "CX3CR1/CX3CL1 axis drives the migration and maturation of oligodendroglia in the central nervous system." Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/29533.
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In the central nervous system, the axons of neurons are protected from damage and aided in electrical conductivity by the myelin sheath, a complex of proteins and lipids formed by oligodendrocytes. Loss or damage to the myelin sheath may result in impairment of electrical axonal conduction and eventually to neuronal death. Such demyelination is responsible, at least in part, for the disabling neurodegeneration observed in pathologies such as Multiple Sclerosis (MS) and Spinal Cord Injury. In the regenerative process of remyelination, oligodendrocyte precursor cells (OPCs), the resident glial stem cell population of the adult CNS, migrate toward the injury site, proliferate and differentiate into adult oligodendrocytes which subsequently reform the myelin sheath. Existing research indicates that OPC migration is directed by chemomigratory signals released from the site of injury and that the absence of OPCs is a feature of some MS lesions, suggesting that increased recruitment of OPCs to injury sites might improve remyelination, eventually leading to treatments of patient pathologies. I hypothesized that as yet undiscovered migration cues for OPCs might be released at sites of demyelination, diffuse through the CNS tissue, activate distal OPCs and guide them back to sites of demyelination. In this thesis, I performed bioinformatics analysis of gene expression arrays and identified upregulated cell surface receptors on OPCs activated in a cuprizone model, and upregulated secreted factors in whole lesion sites from an LPC induced MS type injury model and a Spinal Cord Injury model. I then optimised the X-celligence system for the quantification of OPC migration in response to secreted factors identified in my bioinformatics screen. By combination of these techniques with immunofluorescent staining I discovered novel expression of the cell surface receptor CX3CR1 on OPCs, increased expression of the corresponding ligand CX3CL1 in both MS type injury and Spinal Cord Injury, increased directional migration of OPCs in response to low concentrations of CX3CL1, and increased maturation of OPCs into adult oligodendrocytes at high concentrations of CX3CL1. Taken together these results propose a system in which an increasing gradient of CX3CL1 released from the site of injury directs the recruitment, then maturation of OPCs, making CX3CL1 a master regulator of OPC led CNS regeneration.
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MAURI, MARIO. "Cellule staminali mesenchimali: potenziali modulatori del sistema nervoso centrale." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2012. http://hdl.handle.net/10281/39835.
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Bone marrow-derived mesenchymal stem cells (MSCs) account for a small population of cells of the non-hematopoietic component of bone marrow. MSCs are multipotent stem cells endowed with neurotrophic potential combined to immunological properties, making them a promising therapeutic tool for neurodegenerative disorders. Although the mechanisms by which they act are still largely unknown, trans-differentiation, paracrine and autocrine actions have been hypothesized. Here we focus on the study of the effects exerted by rat MSCs on CNS neurons and oligodendrocytes by using a simplified in vitro co-culture system that precludes any direct contact between different cell types.
The analysis of hippocampal synaptogenesis, synaptic vesicle recycling and electrical activity show that MSCs by themselves, efficiently support morphological and functional neuronal differentiation. Our observations demonstrate that MSCs selectively and directly increased hippocampal GABAergic presynapses and inhibitory transmission. In fact, this increment correlated to a higher expression of the potassium/chloride KCC2 cotransporter and to an enhancement of both the frequency and the amplitude of mIPSC and sIPSC. The decreased of GABA synapses following the treatment with a widely used Trk-neurotrophin receptor blocker, K252a, and the more specific TrkB receptor bodies prompt for the involvement of the brain derived neurotrophic factor (BDNF) in mediating such effects. The involvement of this neurotrophin is also strengthened by test ELISA on the culture medium collected from MSC-neuron co-cultures in which an higher BDNF concentration was detected, when compared to astrocyte-neuron co-cultures.
The results obtained indicate that MSC-secreted factors induce glial-dependent neuronal survival and directly trigger an augmented GABAergic transmission in hippocampal cultures, highlighting a new effect by which MSCs could cooperate in CNS repair.
Additionally, MSCs have been described to improve the clinical course of some demyelinating pathologies and to promote tissue repair through immunological mechanisms and neuroprotective effects. Following these evidences we performed in vitro and in vivo experiments to assess whether MSCs exert their actions through the support of oligodendrocytes (OLs), the myelinating CNS cells, and participate in the regulation of their proliferation and maturation. Through the analysis of specific proteins typically used as markers of the different stages of proliferation, maturation and differentiation (specifically, the membrane glycoprotein O4, the proteoglycan NG2 and myelin basic protein MBP, respectively), it has been noticed that MSCs are capable to prolong the proliferation phase of OPCs and also to anticipate OL differentiation, with respect to standard astrocyte/OL co-cultures. Moreover we investigated a possible molecular mechanism underlying these phenomena focusing on neurotrophin pathways. Trk receptors activation was analyzed in order to find out a possible role of neurotrophins in MSC-mediated effects on OLs, as it happens in neuronal cultures. We focused on the changes in the phosphorylation level of ERK (Extracellular signaling-regulated kinases), one of the activated effectors by TrK receptors. Our observations show that, in OLs co-cultured with MSCs, ERK is highly phosphorylated with respect to astrocyte/OL co-cultures, suggesting a MSC-induced activation of the pathways regulated by this protein. These data, although preliminary, suggest that MSCs positively act on the regulation of proliferation and maturation of OLs and, due to the observed effects on the regulation of synaptogenesis (see above), make these cells an interesting model for the identification of molecules involved in MSC neuroprotective processes. This may open new therapeutic approaches in the treatment of neurodegenerative diseases involving not only a synaptic imbalance, as it happens in various forms of epilepsy, but also in demyelinating diseases. Thus, in this research project, we aimed at characterising the molecular mechanisms underlying MSC actions that could participate in the recovery of neurological disorders or demyelinating pathologies.
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Mohamed, Esraa M. "ENDOGENOUS OPIOID PEPTIDES AND BRAIN DEVELOPMENT: ENDOMORPHIN-1 AND NOCICEPTIN PLAY A SEX-SPECIFIC ROLE IN THE CONTROL OF OLIGODENDROCYTE MATURATION AND BRAIN MYELINATION." VCU Scholars Compass, 2019. https://scholarscompass.vcu.edu/etd/5984.
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Myelin is an extensive cell membrane produced by oligodendrocytes to ensheath neuronal axons in the central nervous system with the primary goal of maximizing the efficiency of electrochemical impulse transmission. During brain development, oligodendrocytes differentiate into myelin forming cells in a tightly regulated process which makes them vulnerable to multiple insults. Previous results from the laboratory showed that the timing of oligodendrocyte differentiation and rat brain myelination were altered by perinatal exposure to buprenorphine and methadone, opioid analogues used for treating pregnant addicts. The mechanism by which these opioids exerted their effects involved two opioid receptors, the μ-opioid receptor (MOR) and the nociceptin/orphanin FQ receptor (NOR). However, the role of these receptors and their endogenous ligands in controlling the timing of myelination under normal physiological conditions of brain development is not known. In this dissertation, we found that the endogenous MOR ligand endomorphin-1 (EM-1) acts as a strong promoter of rat pre-oligodendrocyte differentiation, but surprisingly, this effect is observed only in cells isolated from female pups. Interestingly, the stimulatory action of EM-1 was abolished upon co-incubation with the endogenous NOR ligand, nociceptin. Moreover, injections of NOR antagonist to 9-day-old female and male rat pups accelerated rat brain myelination in female rat pups with no significant changes in their male counterparts. Interestingly, the lack of major sex-dependent differences in developmental brain levels of EM-1 and nociceptin and the presence of the two receptors MOR and NOR in male and female oligodendrocytes suggested that the observed sex-specific responses may be highly dependent on critical intrinsic sex-dependent differences within these cells. Although nociceptin alone did not exert observable effects on pre-oligodendrocyte maturation, it increased the number of cells expressing Ki-67, a cell proliferation indicator, in oligodendrocyte progenitor cultures. These results suggest that nociceptin may be playing a stage specific role in oligodendrocyte development during brain maturation. The finding of critical functions of EM-1 and nociceptin in the developing female oligodendrocytes and brain myelination highlights the need for considering sexual dimorphism in the design of safer and more effective therapeutic approaches for treating opioid abuse, pain, and demyelinating disease as multiple sclerosis.
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Yasuda, Ken. "Effect of fingolimod on oligodendrocyte maturation under prolonged cerebral hypoperfusion." Kyoto University, 2020. http://hdl.handle.net/2433/253172.
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Lafrenaye, Audrey. "Focal adhesion kinase, a major regulator of oligodendrocyte morphological maturation and myelination." VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/53.
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The formation of the myelin sheath is a crucial step during development because it enables fast and efficient propagation of signals within the limited space of the mammalian central nervous system. During the process of myelination, oligodendrocytes actively interact with the extracellular matrix (ECM). These interactions are considered crucial for proper and timely completion of the myelin sheath. However, the exact regulatory circuits involved in the signaling events that occur between the ECM and oligodendrocytes are currently not fully understood. Therefore, in this dissertation we investigated the role of a known integrator of cell-ECM signaling, namely, focal adhesion kinase (FAK), during oligodendrocyte morphological maturation in vivo and in vitro. Conditional and inducible FAK-knockout mice (Fakflox/flox: PLP/CreERT mice) were generated to observe the effect of FAK loss on myelination in vivo. The role of FAK during post-migratory premyelinating oligodendrocyte morphological maturation was explored in vitro using primary rat oligodendrocyte cultures in combination with siRNA or inhibitor treatment. When inducing FAK knockout just prior to and during active myelination in vivo, we observed a significant reduction in the number of myelinated fibers following initial myelination. In addition, our data revealed a decreased number of primary processes extending from oligodendrocyte cell bodies at this stage of development under induction of FAK knockout. In contrast, myelination appeared normal on postnatal day 28. Our in vitro data demonstrated that reduction of FAK expression or activity affected the oligodendrocyte process network maturation in a way that is unique to the ECM substrate present. More specifically, our data suggest that FAK restrains the expansion of the oligodendrocyte process network in the presence of fibronectin and promotes expansion of the oligodendrocyte process network in the presence of laminin-2. We showed that the FAK-mediated restriction of oligodendrocyte morphological maturation is tightly developmentally regulated; being highly active during early stages of post-migratory premyelinating oligodendrocyte morphological maturation but greatly diminished at the later stages of oligodendrocyte development. Thus, our data suggest that FAK controls the efficiency and timing of CNS myelination during its initial stages, at least in part, by regulating oligodendrocyte process network morphological maturation.
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Waggener, Christopher. "Calcium/Calmodulin-Dependent Protein Kinase II Beta (CaMKIIβ): A Regulator of Oligodendrocyte Maturation and Myelination." VCU Scholars Compass, 2013. http://scholarscompass.vcu.edu/etd/527.
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Oligodendrocytes are cells located in the central nervous system (CNS) that are responsible for the production of the lipid rich membrane, myelin. Myelin and the process of making and wrapping myelin around an axon (also known as myelination) are critical for normal development since they ensure proper signal conduction in the vertebrate CNS. The loss or damage of this myelin, which is typically associated with the demyelinating disease multiple sclerosis (MS), is associated with improper axonal protection along with disrupted nerve signaling which can lead to a variety of different debilitating phenotypic responses. It has been shown that there are MS lesions in which oligodendrocyte progenitors are present. However, while these cells are thought to possess the intrinsic ability to myelinate, they do not efficiently mature and/or repair the myelin sheath within the MS lesion. The reasons for this block in differentiation are currently not fully understood. A critical and thorough understanding of oligodendrocyte ix development provides the foundation needed for future research to potentially provide therapeutic targets for stimulating proper maturation and efficient remyelination from the oligodendrocyte progenitors that are present within the MS brain. In the search for regulators of oligodendrocyte development and potential therapeutic targets, the data generated as part of my thesis provided evidence that CaMKII (more specifically CaMKIIβ) is a regulator of oligodendrocyte myelination and maturation. Using pharmacological inhibitors or siRNA-mediated knockdown of this protein resulted in improper formation of the oligodendrocyte process network. Interestingly, siRNA-mediated knockdown of CaMKIIβ appeared to play no noticeable role in the genetic regulation of specific oligodendrocyte developmental markers. Furthermore, an overall reduction of the thickness of the compact myelin was observed in the ventral spinal cord of CaMKIIβ knockout mice. These findings emphasize the importance of CaMKIIβ in oligodendrocyte myelination and maturation. To further investigate CaMKIIβ’s role in the regulation of CNS myelination, the effect of glutamate signaling on CaMKIIβ and in particular its actin binding site were assessed. These data showed that signaling via glutamate transporters promote an increase of process network in oligodendrocytes. This effect was associated with a transient increase in intracellular calcium concentration and a change in the phosphorylation of at least one serine residue present within CaMKIIβ’s actin binding site. Changes in phosphorylation of CaMKIIβ’s actin binding site suggested that CaMKIIβ detaches from filamentous F-actin and x allows for remodeling of the oligodendrocyte’s actin cytoskeleton. This was demonstrated by overexpressing CaMKIIβ actin binding mutant constructs to alter phosphorylation of serine residues to either always allow actin binding (CaMKIIβallA) or never allow actin binding (CaMKIIβallD). The overexpression of CaMKIIβallD alone demonstrated a decrease in the process network of oligodendrocytes and inhibited the effect of glutamate on the process network. In contrast, the overexpression of CaMKIIβallA and CaMKIIβWT alone showed normal process network formation along with a significant increase in the process network after stimulation of glutamate. The above data strongly suggest that there is a significant relationship between sodium dependent glutamate transporters/CaMKIIβ activation and the oligodendrocyte cytoskeleton in the role of regulation of oligodendrocyte differentiation and CNS myelination. The data presented in this dissertation provides overwhelming evidence that CaMKIIβ plays a significant role in the proper formation of the oligodendrocyte complex process network and myelination. CaMKIIβ’s relationship with glutamate and the actin cytoskeleton could lay the foundation for future research not only for the signaling of oligodendrocyte process formation and remyelination but also for future targets for MS therapies.
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Bohassan, Maruah Hejey. "Role of GPR17 in Thrombocyte Aggregation in Adult Zebrafish." Thesis, University of North Texas, 2015. https://digital.library.unt.edu/ark:/67531/metadc822797/.
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GPR17, a uracil nucleotide cysteinyl leukotriene receptor, belongs to the GPCR (G protein coupled receptor) family. It has been shown recently that inhibiting this protein in the nervous system in mice can lead to blockage of oligodendrocyte maturation, which supports myelin repair. Interestingly, our laboratory found GPR17 in thrombocytes. However, we do not know whether it has any function in thrombocyte aggregation or the nature of the ligand. In this paper, we studied the role of GPR17 in hemostasis, which is a fundamental defense mechanism in the event of injury. Using zebrafish as a model system, our laboratory has studied specifically thrombocytes, which play a significant role in hemostasis. The major reasons to use zebrafish as a model system are that their thrombocytes are functionally equivalent to human platelets, the adult fish are amenable to knockdown experiments, and they are readily available in the market. This study was performed by using a piggy back knockdown method where we used a chemical hybrid of control morpholino and an antisense oligonucleotide sequence leads to the degradation the mRNA for GPR17. After knockdown GPR17 in thrombocytes, the percent difference of the thrombocytes aggregation between the control and knockdown blood samples was measured by flow cytometry. We used various thrombocyte agonists to study differences in aggregation between the control and knockdown blood samples. The study showed that knockdown of GPR17 resulted in no significant differences in percent thrombocyte aggregation between control and agonist treated samples except for a slight increase in collagen-treated samples. Thus, it appears that GPR17 has no significant role in hemostasis.
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Houston, Sara Ann. "Signal-Mediated Epigenetic Regulation of Oligodendrocyte Differentiation and Maturation via Alterations in Histone Acetylation Patterns: Implications for Multiple Sclerosis." Kent State University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=kent1414756744.
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HANTAZ-AMBROISE, DJENNET. "Differenciation des cellules de la moelle epiniere de rat in vitro : regulation de la croissance neuritique et de la maturation des cellules gliales." Paris 6, 1988. http://www.theses.fr/1988PA066653.
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L'etude in vitro de cellules neuronales obtenues a partir de cellules primaires de moelle epiniere d'embryons de rat de 14 jours a permis de montrer l'influence, sur la croissance des neurites, de plusieurs facteurs extracellulaires. Les resultats montrent que les neurones spinaux sont capables de repondre a ces differents facteurs par induction de plusieurs formes de croissance neuritique. Les cellules non neuronales jouent un role dans la regulation de ces differentes formes de croissance des neurites
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O'Neill, Sharon M. "Elucidating the role of serine protease kallikrein 6 in oligodendrocyte maturation & myelination." Thesis, 2018. https://hdl.handle.net/2144/29954.
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Multiple sclerosis (MS) is a chronic central nervous system disease featuring exacerbations of inflammation and demyelination that cause progressively debilitating clinical effects over time. Current treatments for multiple sclerosis are limited in their ability to impact overall disease progression. Research aimed at generation of novel potential therapeutics for MS is needed. Recently, kallikrein 6 (KLK6), a member of the kallikrein (KLK) family of secreted serine proteases, was found to be elevated in the cerebrospinal fluid and brain of MS patients. The fifteen known tissue-based KLKs cleave proteins through a similar mechanism, but have different binding pocket specificity, diverse localization in human tissues, and multiple biological functions. KLKs have been linked to normal human physiology (e.g. KLK4, enamel formation) and disease (e.g. KLK3, prostate cancer). KLK6 is one of the highest expressed serine proteases in the healthy human brain and is expressed predominately in mature oligodendrocytes in both human and mouse brain. The role of KLK6 in oligodendrocyte maturation, myelination, and disease is not fully understood.
To evaluate the role of KLK6 in oligodendrocyte maturation, I used a pluripotent in vitro primary cell system to assess the impact of exogenous KLK6 and modulators of the KLK6 pathway on oligodendrocyte maturation. I demonstrate that signaling through KLK6 decreases the number of mature oligodendrocytes in culture, whereas blockade of KLK6 signaling increases the number of mature oligodendrocytes in culture in the presence of triiodothyronine higher than either agent alone. This work suggests that KLK6 modulation impacts oligodendrocyte maturation. To understand the potential impact of KLK6 pathway inhibition on remyelination, I used the toxin cuprizone to induce demyelination in mice. I found that animals treated with a KLK6 inhibitor had increased myelin staining in the corpus callosum compared to vehicle-treated. This work suggests that KLK6 modulates oligodendrocyte maturation and myelination and may be relevant for improving myelin-related therapeutic outcomes, particularly in multiple sclerosis.2019-06-12T00:00:00Z
Book chapters on the topic "Oligodendrocytes maturation"
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Stoffel, Wilhelm. "The Function of Oligodendrocytes in the Maturation of the Brain." In Cellular Metabolism of the Arterial Wall and Central Nervous System, 55–76. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-84949-7_3.
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Seabra, Gabriela, Valéria de Almeida, and Daniel Martins-de-Souza. "Maturation of a Human Oligodendrocyte Cell Line." In Methods in Molecular Biology, 113–21. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8994-2_11.
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Tanaka, K., S. Nogawa, D. Ito, S. Suzuki, T. Dembo, A. Kosakai, and Y. Fakuuchi. "Activation of NG2-Positive Oligodendrocyte Progenitor Cells after Focal Ischemia in Rat Brain." In Maturation Phenomenon in Cerebral Ischemia V, 285–96. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18713-1_29.
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Victoria Sánchez-Gómez, Maria, Mari Paz Serrano, Elena Alberdi, Fernando Pérez-Cerdá, and Carlos Matute. "Isolation, Expansion, and Maturation of Oligodendrocyte Lineage Cells Obtained from Rat Neonatal Brain and Optic Nerve." In Methods in Molecular Biology, 95–113. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7862-5_8.
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