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Reactive astrocytes express the potassium channel K ir4.1 in active multiple sclerosis lesions
Author(s) -
Satoh Junichi,
Tabunoki Hiroko,
Ishida Tsuyoshi,
Saito Yuko,
Konno Hidehiko,
Arima Kunimasa
Publication year - 2013
Publication title -
clinical and experimental neuroimmunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.297
H-Index - 15
ISSN - 1759-1961
DOI - 10.1111/cen3.12011
Subject(s) - multiple sclerosis , microglia , pathology , lesion , neuromyelitis optica , immunohistochemistry , aquaporin 4 , tumor necrosis factor alpha , medicine , biology , inflammation , immunology
Objectives Kir4.1, an inwardly rectifying potassium channel expressed on perivascular and perisynaptic end‐feet of astrocytes, plays a pivotal role in the spatial buffering of the potassium in the brain. A recent study showed that autoantibodies directed to Kir4.1 are detectable in the serum derived from approximately half of the patients with multiple sclerosis ( MS ) and clinically isolated syndrome, although their pathogenic roles should be elucidated. Methods We studied Kir4.1 expression in MS and control brains by immunohistochemistry. Results We found that reactive astrocytes expressed an intense immunoreactivity for Kir4.1 in active demyelinating lesions of MS , active lesion edges of neuromyelitis optica, ischemic lesion edges of cerebral infarction and neurodegenerative lesions of Alzheimer's disease. Reactive astrocytes accumulated in active MS lesions coexpressed Kir4.1 and AQP 4. A subset of amyloid plaques in Alzheimer's disease brains also expressed Kir4.1. In contrast, infiltrating macrophages, activated microglia and surviving oligodendrocytes in active MS lesions did not express Kir4.1. Furthermore, cultured human astrocytes expressed Kir4.1, and the expression levels were not altered by exposure to tumor necrosis factor‐α or interleukin‐1β, but were elevated by transforming growth factor‐β1. Conclusions These results show that reactive astrocytes abundantly express Kir4.1, and Kir4.1 immunoreactivity is not lost in active demyelinating lesions of MS .