کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2167145 1092310 2013 9 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Downregulation of water channel aquaporin-4 in rats with experimental autoimmune encephalomyeritis induced by myelin basic protein
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی بیولوژی سلول
پیش نمایش صفحه اول مقاله
Downregulation of water channel aquaporin-4 in rats with experimental autoimmune encephalomyeritis induced by myelin basic protein
چکیده انگلیسی

Characteristics of myelin basic protein (MBP)-induced experimental autoimmune encephalomyelitis (EAE) include acute edema and infiltration of mononuclear cells (MNCs) in the microvessels of central nervous system (CNS). Aquaporin-4 (AQP4) is a water channel protein expressed in astrocytes foot process throughout the CNS. We performed immunostaining, western blotting and semi-quantitative real-time RT-PCR of AQP4 and glial fibrillary acidic protein (GFAP) in CNS from rats immunized with MBP. Immunohistochemical analysis revealed that AQP4 is down-regulated in MNCs infiltrated microvessels of rats with EAE. Furthermore, western blotting and real-time RT-PCR analyses showed that AQP4 was significantly decreased at the stage of severe EAE compared with control rats. On the other hand, expression of GFAP-protein was significantly increased after stage of severe EAE. Our findings suggest that AQP4 may be involved in forming edema in the inflammatory lesions of EAE accompanying with up-regulation of reactive astrocyte.


► We investigated expression of AQP4 in the spinal cord of rats immunized with MBP.
► AQO4 was histologically down-regulated in inflammatory microvessels of rats with EAE.
► Protein levels and mRNA of AQP4 were significantly decreased at the severe stage.
► Expression of GFAP-protein was significantly increased after stage of severe EAE.
► AQP4 may be involved in forming edema in the inflammatory lesions of EAE.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cellular Immunology - Volume 281, Issue 1, January 2013, Pages 91–99
نویسندگان
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