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Biochimie. 2018 Oct;153:56-69. doi: 10.1016/j.biochi.2018.02.008. Epub 2018 Feb 17.

Modulation of Kv3.1b potassium channel level and intracellular potassium concentration in 158N murine oligodendrocytes and BV-2 murine microglial cells treated with 7-ketocholesterol, 24S-hydroxycholesterol or tetracosanoic acid (C24:0).

Author information

1
Univ. Bourgogne Franche-Comté, Team 'Biochemistry of the Peroxisome, Inflammation and Lipid Metabolism', EA 7270/INSERM, Dijon, France; Univ. Tunis El Manar - Pasteur Institut, Lab, 'Venoms & Therapeutic Biomolecules', Tunis, Tunisia.
2
Univ. Tunis El Manar - Pasteur Institut, Lab, 'Venoms & Therapeutic Biomolecules', Tunis, Tunisia.
3
Univ. Bourgogne Franche-Comté, Team 'Biochemistry of the Peroxisome, Inflammation and Lipid Metabolism', EA 7270/INSERM, Dijon, France; Univ. Monastir, LR12ES05, Lab-NAFS 'Nutrition - Functional Food & Vascular Health', Monastir, Tunisia.
4
Univ. Monastir, LR12ES05, Lab-NAFS 'Nutrition - Functional Food & Vascular Health', Monastir, Tunisia.
5
Swansea Univ. Medical School, ILS1 Building, Singleton Park, Swansea, UK.
6
Univ. Bourgogne Franche-Comté, Team 'Biochemistry of the Peroxisome, Inflammation and Lipid Metabolism', EA 7270/INSERM, Dijon, France.
7
Univ. Lorraine, LCPMC-A2, ICPM, Dept of Chemistry, Metz, France.
8
Dept. Neurology, Hôpital de Hautepierre, Strasbourg, France.
9
Dept. Neurology, Univ. Hospital of Dijon, Univ. Bourgogne Franche-Comté / EA7270, Dijon, France.
10
Univ. Bourgogne Franche-Comté, Team 'Biochemistry of the Peroxisome, Inflammation and Lipid Metabolism', EA 7270/INSERM, Dijon, France. Electronic address: gerard.lizard@u-bourgogne.fr.

Abstract

Little is known about K+ regulation playing major roles in the propagation of nerve impulses, as well as in apoptosis and inflammasome activation involved in neurodegeneration. As increased levels of 7-ketocholesterol (7KC), 24S-hydroxycholesterol (24S-OHC) and tetracosanoic acid (C24:0) have been observed in patients with neurodegenerative diseases, we studied the effect of 24 and/or 48 h of treatment with 7KC, 24S-OHC and C24:0 on Kv3.1b potassium channel level, intracellular K+ concentration, oxidative stress, mitochondrial dysfunction, and plasma membrane permeability in 158N oligodendrocytes and BV-2 microglial cells. In 158N cells, whereas increased level of Kv3.1b was only observed with 7KC and 24S-OHC but not with C24:0 at 24 h, an intracellular accumulation of K+ was always detected. In BV-2 cells treated with 7KC, 24S-OHC and C24:0, Kv3.1b level was only increased at 48 h; intracellular K+ accumulation was found at 24 h with 7KC, 24S-OHC and C24:0, and only with C24:0 at 48 h. Positive correlations between Kv3.1b level and intracellular K+ concentration were observed in 158N cells in the presence of 7KC and 24S-OHC, and in 7KC-treated BV-2 cells at 48 h. Positive correlations were also found between Kv3.1b or the intracellular K+ concentration, overproduction of reactive oxygen species, loss of transmembrane mitochondrial potential and increased plasma membrane permeability in 158N and BV-2 cells. Our data support that the lipid environment affects Kv3.1b channel expression and/or functionality, and that the subsequent rupture of K+ homeostasis is relied with oligodendrocytes and microglial cells damages.

KEYWORDS:

158N cells; 24S-hydroxycholesterol; 7-Ketocholesterol; BV-2 cells; Kv3.1b; Oxysterols; Potassium; Tetracosanoic acid (C24:0)

PMID:
29462682
DOI:
10.1016/j.biochi.2018.02.008
[Indexed for MEDLINE]

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