The Potassium Channel Kv1.5 Expression Alters During Experimental Autoimmune Encephalomyelitis.


Journal

Neurochemical research
ISSN: 1573-6903
Titre abrégé: Neurochem Res
Pays: United States
ID NLM: 7613461

Informations de publication

Date de publication:
Dec 2019
Historique:
received: 23 07 2019
accepted: 11 10 2019
revised: 23 09 2019
pubmed: 19 10 2019
medline: 31 3 2020
entrez: 19 10 2019
Statut: ppublish

Résumé

Multiple sclerosis (MS) is a chronic, inflammatory, neurodegenerative disease with an autoimmune component. It was suggested that potassium channels, which are involved in crucial biological functions may have a role in different diseases, including MS and its animal model, experimental autoimmune encephalomyelitis (EAE). It was shown that voltage-gated potassium channels Kv1.5 are responsible for fine-tuning in the immune physiology and influence proliferation and differentiation in microglia and astrocytes. Here, we explored the cellular distribution of the Kv1.5 channel, together with its transcript and protein expression in the male rat spinal cord during different stages of EAE. Our results reveal a decrease of Kv1.5 transcript and protein level at the peak of disease, where massive infiltration of myeloid cells occurs, together with reactive astrogliosis and demyelination. Also, we revealed that the presence of this channel is not found in infiltrating macrophages/microglia during EAE. It is interesting to note that Kv1.5 channel is expressed only in resting microglia in the naïve animals. Predominant expression of Kv1.5 channel was found in the astrocytes in all experimental groups, while some vimentin

Identifiants

pubmed: 31624998
doi: 10.1007/s11064-019-02892-4
pii: 10.1007/s11064-019-02892-4
doi:

Substances chimiques

Kcna5 protein, rat 0
Kv1.5 Potassium Channel 0
RNA, Messenger 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

2733-2745

Subventions

Organisme : Ministarstvo Prosvete, Nauke i Tehnološkog Razvoja
ID : III41014

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Auteurs

I Bozic (I)

Department of Neurobiology, Institute for Biological Research "Siniša Stanković"- National Institute of Republic of Serbia, University of Belgrade, Belgrade, Serbia.

D Savic (D)

Department of Neurobiology, Institute for Biological Research "Siniša Stanković"- National Institute of Republic of Serbia, University of Belgrade, Belgrade, Serbia.

A Milosevic (A)

Department of Neurobiology, Institute for Biological Research "Siniša Stanković"- National Institute of Republic of Serbia, University of Belgrade, Belgrade, Serbia.

M Janjic (M)

Department of Neurobiology, Institute for Biological Research "Siniša Stanković"- National Institute of Republic of Serbia, University of Belgrade, Belgrade, Serbia.

D Laketa (D)

Department for General Physiology and Biophysics, Faculty of Biology, University of Belgrade, Belgrade, Serbia.

K Tesovic (K)

Department of Neurobiology, Institute for Biological Research "Siniša Stanković"- National Institute of Republic of Serbia, University of Belgrade, Belgrade, Serbia.

I Bjelobaba (I)

Department of Neurobiology, Institute for Biological Research "Siniša Stanković"- National Institute of Republic of Serbia, University of Belgrade, Belgrade, Serbia.

M Jakovljevic (M)

Department of Neurobiology, Institute for Biological Research "Siniša Stanković"- National Institute of Republic of Serbia, University of Belgrade, Belgrade, Serbia.

N Nedeljkovic (N)

Department for General Physiology and Biophysics, Faculty of Biology, University of Belgrade, Belgrade, Serbia.

S Pekovic (S)

Department of Neurobiology, Institute for Biological Research "Siniša Stanković"- National Institute of Republic of Serbia, University of Belgrade, Belgrade, Serbia.

I Lavrnja (I)

Department of Neurobiology, Institute for Biological Research "Siniša Stanković"- National Institute of Republic of Serbia, University of Belgrade, Belgrade, Serbia. irenam@ibiss.bg.ac.rs.

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Classifications MeSH