Journal article
Functional role of endogenous Kv1.4 in experimental demyelination
Journal of neuroimmunology, Vol.343, pp.577227-577227
06/15/2020
DOI: 10.1016/j.jneuroim.2020.577227
PMID: 32247877
Abstract
During neuroinflammation, the shaker type potassium channel Kv1.4 is re-expressed in oligodendrocytes (Ol), but not immune cells. Here, we analyze the role of endogenous Kv1.4 in two demyelinating animal models of multiple sclerosis. While Kv1.4 deficiency in primary murine Ol led to a decreased proliferation rate in vitro, it did not exert an effect on Ol proliferation or on the extent of de- or remyelination in the cuprizone model in vivo. However, in experimental autoimmune encephalomyelitis, Kv1.4(-/-) mice exhibited a milder disease course and reduced Th1 responses. These data argue for an indirect effect of Kv1.4 on immune cells, possibly via glial cells.
Details
- Title: Subtitle
- Functional role of endogenous Kv1.4 in experimental demyelination
- Creators
- Maria Nazareth Gonzalez-Alvarado - University of Erlangen-NurembergCaroline Roetger - Friedrich Alexander Univ Erlangen Nuremberg, Univ Hosp Erlangen, Dept Neurol, Erlangen, GermanyLaura Berger - University of Erlangen-NurembergBarry London - Roy J. and Lucille A. Carver College of MedicineStefanie Haase - University of RegensburgKristina Kuhbandner - University of Erlangen-NurembergDe-Hyung Lee - University of RegensburgRalf A. Linker - University of Regensburg
- Resource Type
- Journal article
- Publication Details
- Journal of neuroimmunology, Vol.343, pp.577227-577227
- Publisher
- Elsevier
- DOI
- 10.1016/j.jneuroim.2020.577227
- PMID
- 32247877
- ISSN
- 0165-5728
- eISSN
- 1872-8421
- Number of pages
- 10
- Grant note
- 270949263/GRK2162 / Deutsche Forschungsgemeinschaft (DFG, German Research Foundation); German Research Foundation (DFG)
- Language
- English
- Date published
- 06/15/2020
- Academic Unit
- Molecular Physiology and Biophysics; Cardiovascular Medicine; Internal Medicine
- Record Identifier
- 9984297493402771
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