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https://www.readbyqxmd.com/read/29710394/adipose-derived-stem-cells-reduce-fibrosis-and-promote-nerve-regeneration-in-rats
#1
Pietro G di Summa, Luigi Schiraldi, Mario Cherubino, Carlo M Oranges, Daniel F Kalbermatten, Wassim Raffoul, Srinivas Madduri
Peripheral nerve regeneration is critical and challenging in the adult humans. High level of collagen infiltration (i.e., scar tissue), in the niche of injury, impedes axonal regeneration and path finding. Unfortunately, studies focusing on the modulation of scar tissue in the nerves are scarce. To address part of this problem, we have evaluated the differentiated adipose derived stem cells (dASCs) for their anti-fibrotic and regenerative effects in a 10 mm nerve gap model in rats. Three different animal groups (n=5) were treated with fibrin nerve conduits (empty), or seeded with dASCs (F+dASCs) and autograft respectively...
April 30, 2018: Anatomical Record: Advances in Integrative Anatomy and Evolutionary Biology
https://www.readbyqxmd.com/read/29599706/lipoprotein-lipase-is-a-feature-of-alternatively-activated-microglia-and-may-facilitate-lipid-uptake-in-the-cns-during-demyelination
#2
Kimberley D Bruce, Sachi Gorkhali, Katherine Given, Alison M Coates, Kristen E Boyle, Wendy B Macklin, Robert H Eckel
Severe demyelinating disorders of the central nervous system (CNS) such as multiple sclerosis (MS), can be devastating for many young lives. To date, the factors resulting in poor remyelination and repair are not well understood, and reparative therapies that benefit MS patients have yet to be developed. We have previously shown that the activity and abundance of Lipoprotein Lipase (LPL)-the rate-limiting enzyme in the hydrolysis of triglyceride-rich lipoproteins-is increased in Schwann cells and macrophages following nerve crush injury in the peripheral nervous system (PNS), suggesting that LPL may help scavenge myelin-derived lipids...
2018: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/29546706/human-induced-pluripotent-stem-cell-derived-sensory-neurons-for-fate-commitment-of-bone-marrow-stromal-cell-derived-schwann-cells
#3
Sa Cai, Daisy K Y Shum, Ying-Shing Chan
Here we describe the in vitro derivation of sensory neurons for use in effecting fate commitment of Schwann cell-like cells derived from human bone marrow stromal cells (hBMSCs). We adopt a novel combination of small molecules in an 8-day program that induces the differentiation of human induced pluripotent stem cells into sensory neurons. In co-cultures, the derived sensory neurons present contact-dependent cues to direct hBMSC-derived Schwann cell-like cells toward the Schwann cell fate. These derived human Schwann cells survive passaging and cryopreservation, retain marker expression despite withdrawal of glia-inducing medium and neuronal cues, demonstrate capacity for myelination, and therefore promise application in autologous transplantation and re-myelination therapy...
2018: Methods in Molecular Biology
https://www.readbyqxmd.com/read/29513163/electrical-stimulation-promotes-regeneration-and-re-myelination-of-axons-of-injured-facial-nerve-in-rats
#4
Yue Deng, Yaping Xu, Huanhai Liu, Hu Peng, Qilei Tao, Hongyi Liu, Haibin Liu, Jian Wu, Xiaoping Chen, Jingping Fan
Objective To investigate the effects of electrical stimulation (ES) on the nerve regeneration and functional recovery of facial expression muscles in facial nerve defect rats. Methods Sixty rats were surgically introduced with a 1-cm defect on the right facial nerves and evenly divided into the Surgery group (Group A, the main trunk of the right facial nerve was surgically cut-off with a 1.0 cm at the foramina stylomastoideum) and the Surgery + ES group (Group B). Twenty normal rats were as normal control group (without receiving surgery or ES)...
March 2018: Neurological Research
https://www.readbyqxmd.com/read/29315804/white-matter-tauopathy-transient-functional-loss-and-novel-myelin-remodeling
#5
Joshua Jackson, Gabby Bianco, Angelo O Rosa, Katrina Cowan, Peter Bond, Oleg Anichtchik, Robert Fern
Early white matter (WM) changes are common in dementia and may contribute to functional decline. We here examine this phenomenon in an induced dementia model for the first time. We report a novel and selective form of myelin injury as the first manifestation of tauopathy in the adult central nervous system. Myelin pathology rapidly followed the induction of a P301 tau mutation associated with fronto-temporal dementia in humans (rTG4510 line). Damage involved focal disruption of the ad-axonal myelin lamella and internal oligodendrocyte tongue process, followed by myelin remodeling with features of re-myelination that included myelin thinning and internodal shortening...
April 2018: Glia
https://www.readbyqxmd.com/read/29216454/fibrinogen-in-the-nervous-system-glia-beware
#6
Erin H Norris, Sidney Strickland
Re-myelination of CNS nerves after injury is ineffective. Here, Petersen et al. (2017) show that the blood clotting protein fibrinogen inhibits nerve repair by preventing oligodendrocyte progenitor cells from differentiating into myelinating oligodendrocytes. Targeting fibrinogen or its downstream BMP signaling pathway may help with CNS repair.
December 6, 2017: Neuron
https://www.readbyqxmd.com/read/29216327/protamine-neutralizes-chondroitin-sulfate-proteoglycan-mediated-inhibition-of-oligodendrocyte-differentiation
#7
Kazuya Kuboyama, Naomi Tanga, Ryoko Suzuki, Akihiro Fujikawa, Masaharu Noda
Chondroitin sulfate proteoglycans (CSPGs), which are enriched in demyelinating plaques in neurodegenerative diseases, such as multiple sclerosis (MS), impair remyelination by inhibiting the migration and differentiation of oligodendrocyte precursor cells (OPCs) in the central nervous system (CNS). We herein show that protamine (PRM, also known as a heparin antagonist) effectively neutralizes the inhibitory activities of CSPGs, thereby enhancing OPC differentiation and (re)myelination in mice. Cell-based assays using mouse OPC-like OL1 cells revealed that the PRM treatment exerted masking effects on extracellular CSPGs and improved oligodendrocyte differentiation on inhibitory CSPG-coated substrates...
2017: PloS One
https://www.readbyqxmd.com/read/29183776/assessment-of-microstructural-signal-compartments-across-the-corpus-callosum-using-multi-echo-gradient-recalled-echo-at-7-t
#8
Kiran Thapaliya, Viktor Vegh, Steffen Bollmann, Markus Barth
Quantitative assessment of tissue microstructure is important in studying human brain diseases and disorders in which white matter is implicated, as it has been linked to demyelination, re-myelination, and axonal damage in clinical conditions. Ultra-high field magnetic resonance imaging data obtained using a multi-echo gradient echo sequence has been shown to contain information on myelin, axonal and extracellular compartments in white matter. In this study, we aimed to assess the sensitivity of a three-compartment model to estimate the variation of corresponding compartment parameters (water fraction, relaxation time and frequency shift) of the corpus callosum sub-regions, which are known to have different tissue structure...
November 26, 2017: NeuroImage
https://www.readbyqxmd.com/read/29109239/graded-elevation-of-c-jun-in-schwann-cells-in-vivo-gene-dosage-determines-effects-on-development-re-myelination-tumorigenesis-and-hypomyelination
#9
Shaline V Fazal, Jose A Gomez-Sanchez, Laura J Wagstaff, Nicolo Musner, Georg Otto, Martin Janz, Rhona Mirsky, Kristjan R Jessen
Schwann cell c-Jun is implicated in adaptive and maladaptive functions in peripheral nerves. In injured nerves, this transcription factor promotes the repair Schwann cell phenotype and regeneration, and it promotes Schwann cell mediated neurotrophic support in models of peripheral neuropathies. However, c-Jun is associated with tumour formation in some systems, it potentially supresses myelin genes, and has been implicated in demyelinating neuropathies. To clarify these issues, and determine how c-Jun levels determine its function, we have generated, c-Jun OE/+ and c-Jun OE/OE mice, with graded expression of c-Jun in Schwann cells, and examined these lines during development, in adulthood and after injury using RNA sequencing analysis, quantitative electron microscopic morphometry, Western blotting and functional tests...
November 6, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/29080030/progenitors-in-the-ependyma-of-the-spinal-cord-a-potential-resource-for-self-repair-after-injury
#10
Nicolás Marichal, Cecilia Reali, María Inés Rehermann, Omar Trujillo-Cenóz, Raúl E Russo
Traumatic injury of the spinal cord leads to devastating conditions that affect ~2.5 million people worldwide. This is because the mammalian spinal cord reacts to injury with only limited endogenous repair. Functional restoration requires the replacement of lost cells, the growth and navigation of regenerating axons on a permissive scaffold and axon re-myelination. The manipulation of endogenous spinal stem cells is regarded as a potential strategy to restore function. For this type of therapy it is necessary to determine the molecular and functional mechanisms regulating the proliferation, migration and differentiation of adult spinal progenitors...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28966633/transcriptional-inhibition-in-schwann-cell-development-and-nerve-regeneration
#11
REVIEW
Susanne Quintes, Bastian G Brinkmann
Schwann cells, the myelinating glial cells of the peripheral nervous system are remarkably plastic after nerve trauma. Their transdifferentiation into specialized repair cells after injury shares some features with their development from the neural crest. Both processes are governed by a tightly regulated balance between activators and inhibitors to ensure timely lineage progression and allow re-maturation after nerve injury. Functional recovery after injury is very successful in rodents, however, in humans, lack of regeneration after nerve trauma and loss of function as the result of peripheral neuropathies represents a significant problem...
August 2017: Neural Regeneration Research
https://www.readbyqxmd.com/read/28875857/is-there-a-link-between-vitamin-b-and-multiple-sclerosis
#12
REVIEW
Natalie Nemazannikova, Kathleen Mikkelsen, Lily Stojanovska, Gregory L Blatch, Vasso Apostolopoulos
BACKGROUND: Damage to the myelin sheath (demyelination) is one of the main manifestations of multiple sclerosis (MS). Interestingly, both MS and vitamin B deficiencies result in severe myelin degeneration, leading to loss in neuronal signal transmission. OBJECTIVE: Deficiency in vitamin B complex vary, although common symptoms include fatigue, increased oxidative stress, inflammation and demyelination. In particular, vitamin B12 (cobalamin) has had increased attention for its role in the methylation process, involvement in myelination and remyelination, and reversal of MS symptoms...
February 6, 2018: Medicinal Chemistry
https://www.readbyqxmd.com/read/28743796/sox2-expression-in-schwann-cells-inhibits-myelination-in-vivo-and-induces-influx-of-macrophages-to-the-nerve
#13
Sheridan L Roberts, Xin-Peng Dun, Robin D S Doddrell, Thomas Mindos, Louisa K Drake, Mark W Onaitis, Francesca Florio, Angelo Quattrini, Alison C Lloyd, Maurizio D'Antonio, David B Parkinson
Correct myelination is crucial for the function of the peripheral nervous system. Both positive and negative regulators within the axon and Schwann cell function to ensure the correct onset and progression of myelination during both development and following peripheral nerve injury and repair. The Sox2 transcription factor is well known for its roles in the development and maintenance of progenitor and stem cell populations, but has also been proposed in vitro as a negative regulator of myelination in Schwann cells...
September 1, 2017: Development
https://www.readbyqxmd.com/read/28522736/myelin-associated-glycoprotein-inhibits-schwann-cell-migration-and-induces-their-death
#14
Nagarathnamma Chaudhry, Corinne Bachelin, Violetta Zujovic, Melissa Hilaire, Katherine T Baldwin, Rose M Follis, Roman Giger, Bruce D Carter, Anne Baron-Van Evercooren, Marie T Filbin
Remyelination of CNS axons by Schwann cells (SCs) is not efficient, in part due to the poor migration of SCs into the adult CNS. Although it is known that migrating SCs avoid white matter tracts, the molecular mechanisms underlying this exclusion have never been elucidated. We now demonstrate that myelin-associated glycoprotein (MAG), a well known inhibitor of neurite outgrowth, inhibits rat SC migration and induces their death via γ-secretase-dependent regulated intramembrane proteolysis of the p75 neurotrophin receptor (also known as p75 cleavage)...
June 14, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28423529/pif-promotes-brain-re-myelination-locally-while-regulating-systemic-inflammation-clinically-relevant-multiple-sclerosis-m-smegmatis-model
#15
Giuseppe Migliara, Martin Mueller, Alessia Piermattei, Chaya Brodie, Michael J Paidas, Eytan R Barnea, Francesco Ria
Neurologic disease diagnosis and treatment is challenging. Multiple Sclerosis (MS) is a demyelinating autoimmune disease with few clinical forms and uncertain etiology. Current studies suggest that it is likely caused by infection(s) triggering a systemic immune response resulting in antigen/non-antigen-related autoimmune response in central nervous system (CNS). New therapeutic approaches are needed. Secreted by viable embryos, PreImplantation Factor (PIF) possesses a local and systemic immunity regulatory role...
March 28, 2017: Oncotarget
https://www.readbyqxmd.com/read/28288125/regulatory-t-cells-promote-myelin-regeneration-in-the-central-nervous-system
#16
Yvonne Dombrowski, Thomas O'Hagan, Marie Dittmer, Rosana Penalva, Sonia R Mayoral, Peter Bankhead, Samara Fleville, George Eleftheriadis, Chao Zhao, Michelle Naughton, Rachel Hassan, Jill Moffat, John Falconer, Amanda Boyd, Peter Hamilton, Ingrid V Allen, Adrien Kissenpfennig, Paul N Moynagh, Emma Evergren, Bernard Perbal, Anna C Williams, Rebecca J Ingram, Jonah R Chan, Robin J M Franklin, Denise C Fitzgerald
Regeneration of CNS myelin involves differentiation of oligodendrocytes from oligodendrocyte progenitor cells. In multiple sclerosis, remyelination can fail despite abundant oligodendrocyte progenitor cells, suggesting impairment of oligodendrocyte differentiation. T cells infiltrate the CNS in multiple sclerosis, yet little is known about T cell functions in remyelination. We report that regulatory T cells (Treg) promote oligodendrocyte differentiation and (re)myelination. Treg-deficient mice exhibited substantially impaired remyelination and oligodendrocyte differentiation, which was rescued by adoptive transfer of Treg...
May 2017: Nature Neuroscience
https://www.readbyqxmd.com/read/28128219/astrocyte-derived-tissue-transglutaminase-affects-fibronectin-deposition-but-not-aggregation-during-cuprizone-induced-demyelination
#17
Nathaly Espitia Pinzon, Berta Sanz-Morello, John J P Brevé, John G J M Bol, Benjamin Drukarch, Jan Bauer, Wia Baron, Anne-Marie van Dam
Astrogliosis as seen in Multiple Sclerosis (MS) develops into astroglial scarring, which is beneficial because it seals off the site of central nervous system (CNS) damage. However, astroglial scarring also forms an obstacle that inhibits axon outgrowth and (re)myelination in brain lesions. This is possibly an important cause for incomplete remyelination in the CNS of early stage MS patients and for failure in remyelination when the disease progresses. In this study we address whether under demyelinating conditions in vivo, tissue Transglutaminase (TG2), a Ca(2+) -dependent enzyme that catalyses posttranslational modification of proteins, contributes to extracellular matrix (ECM) deposition and/or aggregation...
January 27, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28093710/role-of-oligodendrocyte-dysfunction-in-demyelination-remyelination-and-neurodegeneration-in-multiple-sclerosis
#18
REVIEW
Adriana Octaviana Dulamea
Oligodendrocytes (OLs) are the myelinating cells of the central nervous system (CNS) during development and throughout adulthood. They result from a complex and well controlled process of activation, proliferation, migration and differentiation of oligodendrocyte progenitor cells (OPCs) from the germinative niches of the CNS. In multiple sclerosis (MS), the complex pathological process produces dysfunction and apoptosis of OLs leading to demyelination and neurodegeneration. This review attempts to describe the patterns of demyelination in MS, the steps involved in oligodendrogenesis and myelination in healthy CNS, the different pathways leading to OLs and myelin loss in MS, as well as principles involved in restoration of myelin sheaths...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/27973735/the-role-of-p38alpha-in-schwann-cells-in-regulating-peripheral-nerve-myelination-and-repair
#19
Sheridan L Roberts, Xin-Peng Dun, Gemma Dee, Bethany Gray, Thomas Mindos, David B Parkinson
Myelination in the peripheral nervous system (PNS) is controlled by both positive and negative regulators within Schwann cells to ensure timely onset and correct myelin thickness for saltatory conduction by neurons. Transcription factors such as Sox10, octamer-binding transcription factor 6 (Oct6) and Krox20 form a positive regulatory network, whereas negative regulators such as cJun and Sox2 oppose myelination in Schwann cells. The role of the p38 MAPK pathway has been studied in PNS myelination, but its precise function remains unclear, with both positive and negative effects of p38 activity reported upon both myelination and processes of nerve repair...
April 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/27535761/astrocyte-targeted-production-of-interleukin-6-reduces-astroglial-and-microglial-activation-in-the-cuprizone-demyelination-model-implications-for-myelin-clearance-and-oligodendrocyte-maturation
#20
Filip Petković, Iain L Campbell, Berta Gonzalez, Bernardo Castellano
Multiple sclerosis (MS) is a chronic demyelinating disease of the central nervous system. Interleukin (IL)-6 is a pleiotropic cytokine with a potential role in MS. Here we used transgenic mice with astrocyte-targeted production of IL-6 (GFAP-IL6Tg) to study the effect of IL-6 in the cuprizone-induced demyelination paradigm, which is an experimental model of de- and re-myelination, both hallmarks of MS. Our results demonstrated that cuprizone-treated GFAP-IL6Tg mice showed a significant reduction in astroglial and especially microglial activation/accumulation in the corpus callosum in comparison with the corresponding cuprizone-treated wild type (WT)...
December 2016: Glia
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