The Experts below are selected from a list of 87 Experts worldwide ranked by ideXlab platform
Taekyun Shin - One of the best experts on this subject based on the ideXlab platform.
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enhanced expression of netrin 1 protein in the sciatic nerves of lewis rats with experimental Autoimmune neuritis possible role of the netrin 1 dcc binding pathway in an Autoimmune pns disorder
Journal of Neuroimmunology, 2006Co-Authors: Changjong Moon, Yoh Matsumoto, Hongbing Wang, Taekyun ShinAbstract:Netrin-1 is a chemotropic factor that plays an important role as a survival factor in the adult nervous system. To investigate whether netrin-1 is involved in Autoimmune Injury of the peripheral nervous system (PNS), the temporal expression of netrin-1 protein was analyzed in the sciatic nerves of Lewis rats with experimental Autoimmune neuritis (EAN). Western blot analysis revealed a significant increase in the level of netrin-1 protein in the sciatic nerves of rats on days 11 to 24 post-immunization (p.i.) compared to controls; netrin-1 expression declined by day 30 p.i. Immunohistochemistry revealed that netrin-1 protein was expressed weakly in Schwann cells and vessels in the sciatic nerves of normal and CFA-immunized control rats. In the sciatic nerves of EAN-affected rats, netrin-1 immunoreactivity was increased mainly in the cell membrane and extracellular matrix of OX42-positive macrophages and S100-positive Schwann cells at the peak and recovery phases of EAN. Moreover, the putative netrin-1 receptor, deleted in colorectal cancer (DCC), was expressed mainly in axons, some macrophages, and Schwann cells in EAN-affected sciatic nerves, although the level of protein expression did not change significantly over the course of EAN. We suggest that a significant increase in netrin-1 expression contributes to host cell survival and axon regeneration to counter Autoimmune Injury and inflammation, which may play a role in recovery from EAN-induced paralysis.
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activation of extracellular signal regulated kinases in the sciatic nerves of rats with experimental Autoimmune neuritis
Neuroscience Letters, 2004Co-Authors: Changjong Moon, Kuniko Kohyama, Naoyuki Tanuma, Yoh Matsumoto, Taekyun ShinAbstract:Abstract To investigate whether the phosphorylation of extracellular signal-regulated kinase (ERK) is involved in Autoimmune Injury of the peripheral nervous system (PNS), the expression of phosphorylated ERK (p-ERK) was analyzed in experimental Autoimmune neuritis (EAN) in rats. Western blot analysis showed that the level of p-ERK was increased significantly in the sciatic nerves of rats on days 14 ( p p
Changjong Moon - One of the best experts on this subject based on the ideXlab platform.
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enhanced expression of netrin 1 protein in the sciatic nerves of lewis rats with experimental Autoimmune neuritis possible role of the netrin 1 dcc binding pathway in an Autoimmune pns disorder
Journal of Neuroimmunology, 2006Co-Authors: Changjong Moon, Yoh Matsumoto, Hongbing Wang, Taekyun ShinAbstract:Netrin-1 is a chemotropic factor that plays an important role as a survival factor in the adult nervous system. To investigate whether netrin-1 is involved in Autoimmune Injury of the peripheral nervous system (PNS), the temporal expression of netrin-1 protein was analyzed in the sciatic nerves of Lewis rats with experimental Autoimmune neuritis (EAN). Western blot analysis revealed a significant increase in the level of netrin-1 protein in the sciatic nerves of rats on days 11 to 24 post-immunization (p.i.) compared to controls; netrin-1 expression declined by day 30 p.i. Immunohistochemistry revealed that netrin-1 protein was expressed weakly in Schwann cells and vessels in the sciatic nerves of normal and CFA-immunized control rats. In the sciatic nerves of EAN-affected rats, netrin-1 immunoreactivity was increased mainly in the cell membrane and extracellular matrix of OX42-positive macrophages and S100-positive Schwann cells at the peak and recovery phases of EAN. Moreover, the putative netrin-1 receptor, deleted in colorectal cancer (DCC), was expressed mainly in axons, some macrophages, and Schwann cells in EAN-affected sciatic nerves, although the level of protein expression did not change significantly over the course of EAN. We suggest that a significant increase in netrin-1 expression contributes to host cell survival and axon regeneration to counter Autoimmune Injury and inflammation, which may play a role in recovery from EAN-induced paralysis.
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activation of extracellular signal regulated kinases in the sciatic nerves of rats with experimental Autoimmune neuritis
Neuroscience Letters, 2004Co-Authors: Changjong Moon, Kuniko Kohyama, Naoyuki Tanuma, Yoh Matsumoto, Taekyun ShinAbstract:Abstract To investigate whether the phosphorylation of extracellular signal-regulated kinase (ERK) is involved in Autoimmune Injury of the peripheral nervous system (PNS), the expression of phosphorylated ERK (p-ERK) was analyzed in experimental Autoimmune neuritis (EAN) in rats. Western blot analysis showed that the level of p-ERK was increased significantly in the sciatic nerves of rats on days 14 ( p p
Hugh J. Willison - One of the best experts on this subject based on the ideXlab platform.
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The Effects of Age and Ganglioside Composition on the Rate of Motor Nerve Terminal Regeneration Following Antibody-Mediated Injury in Mice
2016Co-Authors: Angie Rupp, Madeleine E. Cunningham, Denggao Yao, Koichi Furukawa, Hugh J. WillisonAbstract:KEY WORDS antibody; complement; ganglioside; neuromuscular junction; neuropathy ABSTRACT Gangliosides are glycosphingolipids highly enriched in neural plasma membranes, where they mediate a diverse range of functions and can act as targets for auto-antibodies present in human immune-mediated neuropathy sera. The ensuing Autoimmune Injury results in axonal and motor nerve terminal (mNT) degeneration. Both aging and ganglioside-deficiency have been linked to impaired axonal regenera-tion. To assess the effects of age and ganglioside expression on mNT regeneration in an Autoimmune Injury paradigm, anti-ganglioside antibodies and complement were applied to young adult and aged mice wildtype (WT) mice, mice deficient in either b-and c-series (GD3sKO) or mice deficient in all complex gangliosides (GM2sKO). The extent of mNT Injury and regeneration was assessed immediately or after 5 days, respectively. Depending on ganglioside expression and antibody-specificity, either a selective mNT Injury or a combined Injury of mNTs and neuromuscular glial cells was elicited. Immediately after induction of the Injury, between 1.5 % and 11.8 % of neuro
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Gangliosides as targets for Autoimmune Injury to the nervous system.
Journal of Neurochemistry, 2007Co-Authors: Hugh J. WillisonAbstract:Immune responses directed towards gangliosides and their microbial mimics are important mediators of several subtypes of acute post-infectious Autoimmune neuropathy, collectively referred to as the Guillain–Barre syndromes. In this diverse group of paralytic syndromes, the immunopathology is in a proportion of cases characterised by anti-ganglioside antibody deposits, accompanied by inflammatory destruction of both axonal and glial components within the PNS. By gaining an understanding of the immunological mechanisms underlying these pathological pathways, it should be possible to select the correct targets for therapeutic intervention. Recent years has seen particular progress in our understanding of the basis for, and immunological consequences of molecular mimicry between gangliosides and microbial glycans, the relationships between ganglioside antibody specificity and different clinical phenotypes of GBS, the pathological basis for antibody-mediated nerve Injury and the testing of intervention strategies in pre-clinical models. The focus of this mini-review is to provide a brief background to this field, summarise a selection of recent highlights focused on our own research, identify areas of outstanding knowledge and present data that supports novel therapeutic approaches based on the latest experimental findings.
Yoh Matsumoto - One of the best experts on this subject based on the ideXlab platform.
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enhanced expression of netrin 1 protein in the sciatic nerves of lewis rats with experimental Autoimmune neuritis possible role of the netrin 1 dcc binding pathway in an Autoimmune pns disorder
Journal of Neuroimmunology, 2006Co-Authors: Changjong Moon, Yoh Matsumoto, Hongbing Wang, Taekyun ShinAbstract:Netrin-1 is a chemotropic factor that plays an important role as a survival factor in the adult nervous system. To investigate whether netrin-1 is involved in Autoimmune Injury of the peripheral nervous system (PNS), the temporal expression of netrin-1 protein was analyzed in the sciatic nerves of Lewis rats with experimental Autoimmune neuritis (EAN). Western blot analysis revealed a significant increase in the level of netrin-1 protein in the sciatic nerves of rats on days 11 to 24 post-immunization (p.i.) compared to controls; netrin-1 expression declined by day 30 p.i. Immunohistochemistry revealed that netrin-1 protein was expressed weakly in Schwann cells and vessels in the sciatic nerves of normal and CFA-immunized control rats. In the sciatic nerves of EAN-affected rats, netrin-1 immunoreactivity was increased mainly in the cell membrane and extracellular matrix of OX42-positive macrophages and S100-positive Schwann cells at the peak and recovery phases of EAN. Moreover, the putative netrin-1 receptor, deleted in colorectal cancer (DCC), was expressed mainly in axons, some macrophages, and Schwann cells in EAN-affected sciatic nerves, although the level of protein expression did not change significantly over the course of EAN. We suggest that a significant increase in netrin-1 expression contributes to host cell survival and axon regeneration to counter Autoimmune Injury and inflammation, which may play a role in recovery from EAN-induced paralysis.
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activation of extracellular signal regulated kinases in the sciatic nerves of rats with experimental Autoimmune neuritis
Neuroscience Letters, 2004Co-Authors: Changjong Moon, Kuniko Kohyama, Naoyuki Tanuma, Yoh Matsumoto, Taekyun ShinAbstract:Abstract To investigate whether the phosphorylation of extracellular signal-regulated kinase (ERK) is involved in Autoimmune Injury of the peripheral nervous system (PNS), the expression of phosphorylated ERK (p-ERK) was analyzed in experimental Autoimmune neuritis (EAN) in rats. Western blot analysis showed that the level of p-ERK was increased significantly in the sciatic nerves of rats on days 14 ( p p
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microglia intrinsic immuneffector cell of the brain
Brain Research Reviews, 1995Co-Authors: Jochen Gehrmann, Yoh Matsumoto, Georg W KreutzbergAbstract:Abstract Microglia form a regularly spaced network of resident glial cells throughout the central nervous system (CNS). They are morphologically, immunophenotypically and functionally related to cells of the monocyte/macrophage lineage. In the ultimate vicinity of the blood-brain barrier two specialized subsets of macrophages/microglia can be distinguished: firstly, perivascular cells which are enclosed within the basal lamina and secondly juxtavascular microglia which make direct contact with the parenchymal side of the CNS vascular basal lamina but represent true intraparenchymal resident microglia. Bone marrow chimera experiments indicate that a high percentage of the perivascular cells undergoes replacement with bone marrow-derived cells. In contrast, juxtavascular microglia like other resident microglia form a highly stable pool of CNS cells with extremely little turnover with the bone marrow compartment. Both the perivascular cells and the juxtavascular microglia play an important role in initiating and maintaining CNS Autoimmune Injury due to their strategic localization at a site close to the blood-brain barrier, their rapid inducibility for MHC class II antigens and their potential scavenger role as phagocytic cells. The constantly replaced pool of perivascular cells probably represents an entry route by which HIV gets access to the brain. Microglia are the first cell type to respond to several types of CNS Injury. Microglial activation involves a stereotypic pattern of cellular responses, such as proliferation, increased or de-novo expression of immunomolecules, recruitment to the site of Injury and functional changes, e.g., the release of cytotoxic and/or inflammatory mediators. In addition, microglia have a strong antigen presenting function and a pronounced cytotoxic function. Microglial activation is a graded response, i.e., microglia only transform into intrinsic brain phagocytes under conditions of neuronal and or synaptic/terminal degeneration. In T-cell-mediated Autoimmune Injury of the nervous system, microglial activation follows these lines and occurs at an early stage of disease development. In experimental Autoimmune encephalomyelitis (EAE), microglia proliferate vigorously, show a strong expression of MHC class I and II antigens, cell adhesion molecules, release of reactive oxygen intermediates and inflammatory cytokines and transform into phagocytic cells. Due to their pronounced antigen presenting function in vitro, activated microglia rather than astrocytes or endothelial cells are the candidates as intrinsic antigen presenting cel of the brain. In contrast to microglia, astrocytes react with a delay, appear to encase morphologically the inflammatory lesion and may be instrumental in downregulating the T-cell-mediated immune Injury by inducing T-cell apoptosis. In experimental Autoimmune neuritis (EAN), microglial activation occurs also rapidly and operates at long distance, suggesting the involvement of remote and fast signaling mechanisms. During Autoimmune inflammation of the nervous system microglia release as well as respond to several cytokines, including IL-1, IL-6, TNF-α, IFN-γ, TNF-α and TGFβ which are instrumental in astrocyte activation, induction of cell adhesion molecule expression, recruitment of T-cells into the lesion, but also in down-regulating disease progression at later stages. In addition to the synthesis of inflammatory cytokines, microglia act as cytotoxic effector cells by releasing other harmful substances such as proteases, reactive oxygen intermediates and nitric oxide. New therapeutic strategies to reduce the extent of tissue damage in Autoimmune diseases of the nervous system will therefore aim at interfering with microglial cytotoxicity in the early, still potentially reversible stage of tissue damage. In summary, the CNS harbours a network of potential immunoeffector cells, i.e., the microglia, which show a graded response to CNS Injury and function as a sensor to threats in the nervous system.
Hongbing Wang - One of the best experts on this subject based on the ideXlab platform.
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enhanced expression of netrin 1 protein in the sciatic nerves of lewis rats with experimental Autoimmune neuritis possible role of the netrin 1 dcc binding pathway in an Autoimmune pns disorder
Journal of Neuroimmunology, 2006Co-Authors: Changjong Moon, Yoh Matsumoto, Hongbing Wang, Taekyun ShinAbstract:Netrin-1 is a chemotropic factor that plays an important role as a survival factor in the adult nervous system. To investigate whether netrin-1 is involved in Autoimmune Injury of the peripheral nervous system (PNS), the temporal expression of netrin-1 protein was analyzed in the sciatic nerves of Lewis rats with experimental Autoimmune neuritis (EAN). Western blot analysis revealed a significant increase in the level of netrin-1 protein in the sciatic nerves of rats on days 11 to 24 post-immunization (p.i.) compared to controls; netrin-1 expression declined by day 30 p.i. Immunohistochemistry revealed that netrin-1 protein was expressed weakly in Schwann cells and vessels in the sciatic nerves of normal and CFA-immunized control rats. In the sciatic nerves of EAN-affected rats, netrin-1 immunoreactivity was increased mainly in the cell membrane and extracellular matrix of OX42-positive macrophages and S100-positive Schwann cells at the peak and recovery phases of EAN. Moreover, the putative netrin-1 receptor, deleted in colorectal cancer (DCC), was expressed mainly in axons, some macrophages, and Schwann cells in EAN-affected sciatic nerves, although the level of protein expression did not change significantly over the course of EAN. We suggest that a significant increase in netrin-1 expression contributes to host cell survival and axon regeneration to counter Autoimmune Injury and inflammation, which may play a role in recovery from EAN-induced paralysis.
