| Time-dependent changes in proinflammatory and neurotrophic responses of microglia and astrocytes in a rat model of osmotic demyelination syndrome. | |
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MedLine Citation:
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PMID: 21264951 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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Osmotic demyelination syndrome (ODS) is a serious demyelinating disease in the central nervous system usually caused by rapid correction of hyponatremia. In an animal model of ODS, we previously reported microglial accumulation expressing proinflammatory cytokines. Microglia and astrocytes secreting proinflammatory cytokines and neurotrophic factors are reported to be involved in the pathogenesis of demyelinative diseases. Therefore, to clarify the role of microglial and astrocytic function in ODS, we examined the time-dependent changes in distribution, morphology, proliferation, and mRNA/protein expression of proinflammatory cytokines, neurotrophic factors, and matrix metalloproteinase (MMP) in microglia and astrocytes 2 days (early phase) and 5 days (late phase) after the rapid correction of hyponatremia in ODS rats. The number of microglia time dependently increased at demyelinative lesion sites, proliferated, and expressed tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, inducible nitric oxide synthase, and MMP2, 9, and 12 at the early phase. Microglia also expressed leukemia inhibitory factor (a neurotrophic factor) and phagocytosed myelin debris at the late phase. The number of astrocytes time dependently increased around demyelinative lesions, extended processes to lesions, proliferated, and expressed nerve growth factor and glial cell line-derived neurotrophic factor at the late phase. Moreover, treatment with infliximab, a monoclonal antibody against TNF-α, significantly attenuated neurological impairments. Our results suggest that the role of microglia in ODS is time dependently shifted from detrimental to protective and that astrocytes play a protective role at the late phase. Modulation of excessive proinflammatory responses in microglia during the early phase after rapid correction may represent a therapeutic target for ODS. © 2010 Wiley-Liss, Inc. |
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Authors:
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Shintaro Iwama; Yoshihisa Sugimura; Haruyuki Suzuki; Hiromi Suzuki; Takashi Murase; Nobuaki Ozaki; Hiroshi Nagasaki; Hiroshi Arima; Yoshiharu Murata; Makoto Sawada; Yutaka Oiso |
Publication Detail:
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Type: Journal Article Date: 2010-12-29 |
Journal Detail:
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Title: Glia Volume: 59 ISSN: 1098-1136 ISO Abbreviation: Glia Publication Date: 2011 Mar |
Date Detail:
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Created Date: 2011-01-25 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8806785 Medline TA: Glia Country: United States |
Other Details:
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Languages: eng Pagination: 452-62 Citation Subset: IM |
Copyright Information:
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Copyright © 2010 Wiley-Liss, Inc. |
Affiliation:
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Department of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, Nagoya, Japan. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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