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Keratan sulfate expression in microglia is diminished in the spinal cord in experimental autoimmune neuritis
Experimental autoimmune neuritis (EAN) is an animal model of Guillain–Barré syndrome, an inflammatory demyelination disease of the peripheral nervous system. Although this disease has been extensively studied on peripheral nerves, the pathology of the central nervous system has not been fully unders...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3877550/ https://www.ncbi.nlm.nih.gov/pubmed/24309933 http://dx.doi.org/10.1038/cddis.2013.479 |
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author | Matsui, H Ohgomori, T Natori, T Miyamoto, K Kusunoki, S Sakamoto, K Ishiguro, N Imagama, S Kadomatsu, K |
author_facet | Matsui, H Ohgomori, T Natori, T Miyamoto, K Kusunoki, S Sakamoto, K Ishiguro, N Imagama, S Kadomatsu, K |
author_sort | Matsui, H |
collection | PubMed |
description | Experimental autoimmune neuritis (EAN) is an animal model of Guillain–Barré syndrome, an inflammatory demyelination disease of the peripheral nervous system. Although this disease has been extensively studied on peripheral nerves, the pathology of the central nervous system has not been fully understood. Previous studies demonstrate that expression of keratan sulfate (KS), the sugar chain of proteoglycan, is associated with activated microglia/macrophages accumulated after neuronal injuries. Unexpectedly, we found here that KS is rather diminished in rat EAN. KS was restrictively expressed in microglia in the spinal cord of normal rats. KS was positive in 50% microglia in the ventral horn and 20% in the dorsal horn. In EAN, microglia increased in number and expressed the activation marker CD68, but KS expression was abolished. Concomitantly, pro-inflammatory cytokines, i.e., interferon (IFN)-γ, interleukin (IL)-1β, and tumor necrosis factor (TNF)-α, were increased in the spinal cord of EAN rats, whereas anti-inflammatory cytokines, such as IL-4 and IL-10, were decreased. In addition, silencing of KSGal6ST attenuated KS expression on the primary cultured microglia and upregulated expression of some activation markers (TNF-α, IL-1β, and iNOS) under the stimulation with lipopolysaccharide and IFN-γ. This study demonstrates for the first time a close association of EAN and disappearance of KS on microglia. KS expression could be a useful marker to evaluate the status of polyneuropathy. |
format | Online Article Text |
id | pubmed-3877550 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-38775502014-01-02 Keratan sulfate expression in microglia is diminished in the spinal cord in experimental autoimmune neuritis Matsui, H Ohgomori, T Natori, T Miyamoto, K Kusunoki, S Sakamoto, K Ishiguro, N Imagama, S Kadomatsu, K Cell Death Dis Original Article Experimental autoimmune neuritis (EAN) is an animal model of Guillain–Barré syndrome, an inflammatory demyelination disease of the peripheral nervous system. Although this disease has been extensively studied on peripheral nerves, the pathology of the central nervous system has not been fully understood. Previous studies demonstrate that expression of keratan sulfate (KS), the sugar chain of proteoglycan, is associated with activated microglia/macrophages accumulated after neuronal injuries. Unexpectedly, we found here that KS is rather diminished in rat EAN. KS was restrictively expressed in microglia in the spinal cord of normal rats. KS was positive in 50% microglia in the ventral horn and 20% in the dorsal horn. In EAN, microglia increased in number and expressed the activation marker CD68, but KS expression was abolished. Concomitantly, pro-inflammatory cytokines, i.e., interferon (IFN)-γ, interleukin (IL)-1β, and tumor necrosis factor (TNF)-α, were increased in the spinal cord of EAN rats, whereas anti-inflammatory cytokines, such as IL-4 and IL-10, were decreased. In addition, silencing of KSGal6ST attenuated KS expression on the primary cultured microglia and upregulated expression of some activation markers (TNF-α, IL-1β, and iNOS) under the stimulation with lipopolysaccharide and IFN-γ. This study demonstrates for the first time a close association of EAN and disappearance of KS on microglia. KS expression could be a useful marker to evaluate the status of polyneuropathy. Nature Publishing Group 2013-12 2013-12-05 /pmc/articles/PMC3877550/ /pubmed/24309933 http://dx.doi.org/10.1038/cddis.2013.479 Text en Copyright © 2013 Macmillan Publishers Limited http://creativecommons.org/licenses/by/3.0/ This work is licensed under a Creative Commons Attribution 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by/3.0/ |
spellingShingle | Original Article Matsui, H Ohgomori, T Natori, T Miyamoto, K Kusunoki, S Sakamoto, K Ishiguro, N Imagama, S Kadomatsu, K Keratan sulfate expression in microglia is diminished in the spinal cord in experimental autoimmune neuritis |
title | Keratan sulfate expression in microglia is diminished in the spinal cord in experimental autoimmune neuritis |
title_full | Keratan sulfate expression in microglia is diminished in the spinal cord in experimental autoimmune neuritis |
title_fullStr | Keratan sulfate expression in microglia is diminished in the spinal cord in experimental autoimmune neuritis |
title_full_unstemmed | Keratan sulfate expression in microglia is diminished in the spinal cord in experimental autoimmune neuritis |
title_short | Keratan sulfate expression in microglia is diminished in the spinal cord in experimental autoimmune neuritis |
title_sort | keratan sulfate expression in microglia is diminished in the spinal cord in experimental autoimmune neuritis |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3877550/ https://www.ncbi.nlm.nih.gov/pubmed/24309933 http://dx.doi.org/10.1038/cddis.2013.479 |
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