Persistent macrophage/microglial activation and myelin disruption after experimental autoimmune encephalomyelitis in tissue inhibitor of metalloproteinase-1-deficient mice.

Persistent macrophage/microglial activation and myelin disruption after experimental autoimmune encephalomyelitis in tissue inhibitor of metalloproteinase-1-deficient mice. Research Abstract Details 

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Persistent macrophage/microglial activation and myelin disruption after experimental autoimmune encephalomyelitis in tissue inhibitor of metalloproteinase-1-deficient mice. Abstract Text:

Stephen J Crocker,Jason K Whitmire,Ricardo F Frausto,Parntip Chertboonmuang,Paul D Soloway,J Lindsay Whitton,Iain L Campbell,

Increased leukocyte trafficking into the parenchyma during inflammatory responses in the central nervous system (CNS) is facilitated by the extracellular proteolytic activities of matrix metalloproteinases that are regulated, in part, by the endogenous tissue inhibitors of metalloproteinases (TIMPs). In experimental autoimmune encephalomyelitis (EAE), TIMP-1 gene expression is induced in astrocytes surrounding inflammatory lesions in the CNS. The physiological importance of this temporal and spatial relationship is not clear. Herein, we have addressed the functional role of TIMP-1 in a myelin oligodendrocyte glycoprotein (MOG35-55)-induced model of EAE using TIMP-1-deficient (TIMP-1-/-) C57BL/6 mice. Although CD4+ T-cell immune responses to myelin in wild-type (WT) and TIMP-1-/- mice were similar, analysis of CNS tissues from TIMP-1-/- mice after EAE revealed more severe myelin pathology than that of WT mice. This disruption of myelin was associated with both increased lymphocyte infiltration and microglial/macrophage accumulation in the brain parenchyma. These findings suggest that induction of TIMP-1 by astrocytes during EAE in WT mice represents an inherent cytoprotective response that mitigates CNS myelin injury through the regulation of both immune cell infiltration and microglial activation.

Persistent macrophage/microglial activation and myelin disruption after experimental autoimmune encephalomyelitis in tissue inhibitor of metalloproteinase-1-deficient mice. Publishing Authors By Initials

SJ Crocker,JK Whitmire,RF Frausto,P Chertboonmuang,PD Soloway,JL Whitton,IL Campbell,

For similar proteins: tissue inhibitor of metalloproteinases: tissue inhibitor of metalloproteinase-1 research abstracts see: proteins: tissue inhibitor of metalloproteinases: tissue inhibitor of metalloproteinase-1 research

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Persistent macrophage/microglial activation and myelin disruption after experimental autoimmune encephalomyelitis in tissue inhibitor of metalloproteinase-1-deficient mice. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: The American journal of pathology

VOLUME: 169

Page Numbers: 2104-16

Journal Abbreviation: Am. J. Pathol.

ISSN: 0002-9440

DAY: 3

MONTH: Dec

YEAR: 2006

Persistent macrophage/microglial activation and myelin disruption after experimental autoimmune encephalomyelitis in tissue inhibitor of metalloproteinase-1-deficient mice. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 370502

Persistent macrophage/microglial activation and myelin disruption after experimental autoimmune encephalomyelitis in tissue inhibitor of metalloproteinase-1-deficient mice. Keywords Mesh Terms:

KEYWORDS: Tissue Inhibitor of Metalloproteinase-1

MESH TERMS: physiology

Chemical & Substance for Abstract: Persistent macrophage/microglial activation and myelin disruption after experimental autoimmune encephalomyelitis in tissue inhibitor of metalloproteinase-1-deficient mice. Information

Substance Name: oligodendrocyte-myelin glycoprotein

Registry Number: 0

Grant and Affiliation Information for Persistent macrophage/microglial activation and myelin disruption after experimental autoimmune encephalomyelitis in tissue inhibitor of metalloproteinase-1-deficient mice.

AFFILIATION: The Molecular and Integrative Neurosciences Department, The Scripps Research Institute, SP30-2110, 10550 North Torrey Pines Rd., La Jolla, CA 92037, USA. crocker@scripps.edu

Country: United States

AGENCY: United States NINDS

GRANT: NS036979

ACRONYM: NS

MEDLINETA: Am J Pathol

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