Voltage Gated Potassium Channel Kv1.3 Is Upregulated on Activated Astrocytes in Experimental Autoimmune Encephalomyelitis.
2018
Аутори:
Božić, IvaMilošević, Katarina
Laketa, Danijela
Adžić, Marija
Jakovljević, Marija
Bjelobaba, Ivana
Savić, Danijela
Nedeljković, Nadežda
Peković, Sanja
Lavrnja, Irena
Тип документа:
Чланак у часопису (Објављена верзија)
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© 2018 Springer Science+Business Media, LLC, part of Springer Nature
Метаподаци
Приказ свих података о документуАпстракт:
Kv1.3 is a voltage gated potassium channel that has been implicated in pathophysiology of multiple sclerosis (MS). In the present study we investigated temporal and cellular expression pattern of this channel in the lumbar part of spinal cords of animals with experimental autoimmune encephalomyelitis (EAE), animal model of MS. EAE was actively induced in female Dark Agouti rats. Expression of Kv1.3 was analyzed at different time points of disease progression, at the onset, peak and end of EAE. We here show that Kv1.3 increased by several folds at the peak of EAE at both gene and protein level. Double immunofluorescence analyses demonstrated localization of Kv1.3 on activated microglia, macrophages, and reactive astrocytes around inflammatory lesions. In vitro experiments showed that pharmacological block of Kv1.3 in activated astrocytes suppresses the expression of proinflammatory mediators, suggesting a role of this channel in inflammation. Our results support the hypothesis that Kv1.3 may be a therapeutic target of interest for MS and add astrocytes to the list of cells whose activation would be suppressed by inhibiting Kv1.3 in inflammatory conditions.
Кључне речи:
Agitoxin-2; Astrocytes; Experimental autoimmune encephalomyelitis; Neuroinflammation; Voltage gated potassium channel Kv1.3Извор:
Neurochemical Research, 2018, 43, 5, 1020-1034Финансирање / пројекти:
- COST Action BM1406: Ion Channels and Immune Response toward a global understanding of immune cell physiology and for new therapeutic approaches (IONCHAN-IMMUNRESPON)
DOI: 10.1007/s11064-018-2509-8
ISSN: 0364-3190
PubMed: 29574670
WoS: 000432146300005
Scopus: 2-s2.0-85044395801
URI
http://link.springer.com/10.1007/s11064-018-2509-8https://radar.ibiss.bg.ac.rs/handle/123456789/3027