期刊
JOURNAL OF NEUROIMMUNOLOGY
卷 229, 期 1-2, 页码 180-191出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.jneuroim.2010.08.011
关键词
EAE/MS; Tight junctions; Vascular permeability; Blood-brain barrier neuroinflammation
资金
- Multiple Sclerosis Society of Canada Scientific Research Foundation
- Canadian Institiutes of Health Research [VCI-9446]
- Canadian Stroke Metwork [VCI-9446]
- MS Society of Canada
- Dan David Foundation
- UBC/VGH Foundation, University of British Columbia
Multiple sclerosis (MS) is a demyelinating disease characterized by the breakdown of the blood-brain barrier (BBB), and accumulation of inflammatory infiltrates in the central nervous system. Tight junctions are specialized cell-cell adhesion structures and critical components of the BBB that have previously been shown to be abnormally distributed in MS tissue. To evaluate whether experimental autoimmune encephalomyelitis (EAE) provides a suitable model for this aspect of MS disease, we examined the expression and distribution of ZO-1 over the course of disease in EAE. We observed a dramatic relocalization of ZO-1 which precedes overt clinical disease and correlates with the sites of inflammatory cell accumulation. Treatment of in vitro cultures of murine brain endothelial cells with components of EAE induction provided similar findings, with relocalization of ZO-1 and increased permeability of endothelial monolayers. BBB disruption in the EAE model appears to parallel disease progression in MS, with direct effects on the cerebrovascular endothelium, making it an ideal tool for future evaluation of tight junction breakdown and repair in MS-like pathology. (C) 2010 Elsevier B.V. All rights reserved.
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