Accumulation of 24S-hydroxycholesterol in neuronal SK-N-BE cells treated with hexacosanoic acid (C26:0): Argument in favor of 24S-hydroxycholesterol as a potential biomarker of neurolipotoxicity

Zarrouk, Amira; Hammami, Mohamed; Moreau, Thibault; Lizard, Gérard

doi:10.1016/j.neurol.2014.10.016

Cited by 11 publications

(4 citation statements)

References 22 publications

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“…While the underlying mechanism involved in the higher levels of circulating 24OHC in MDD remains unclear, studies have shown that enriched 24OHC levels might lead to many neurotoxic effects, such as inducing oxidative stress, inflammation, apoptosis, and excitatory toxicity ( 33 , 55 , 56 , 57 , 58 , 59 ). Furthermore, previous studies have shown that 24OHC might also serve as a potent positive allosteric modulator for the synaptic excitatory protein NMDA receptor to increase synaptic plasticity ( 60 , 61 , 62 ).…”

Section: Discussionmentioning

confidence: 99%

Tissue-Specific Oxysterols as Predictors of Antidepressant (Escitalopram) Treatment Response in Patients With Major Depressive Disorder

Sun

Yang

Zhou

et al. 2023

Biological Psychiatry Global Open Science

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Section: Discussionmentioning

confidence: 99%

Tissue-Specific Oxysterols as Predictors of Antidepressant (Escitalopram) Treatment Response in Patients With Major Depressive Disorder

Sun

Yang

Zhou

et al. 2023

Biological Psychiatry Global Open Science

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“…Excess accumulation of 24S-HC may promote oxidative stress and cytotoxicity [191,192]. 24S-HC may also be involved in the pathogenesis of neurodegenerative disorders and could be a suitable biomarker for such conditions, as its level reflects the number of metabolically active neurons in the brain [193,194].…”

Section: S-hcmentioning

confidence: 99%

Balancing cholesterol in the brain: from synthesis to disposal

Qian

Chai

Gelissen

et al. 2022

Explor Neuroprot Ther

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The cholesterol is a vital component of cell membranes and myelin sheaths, and a precursor for essential molecules such as steroid hormones. In humans, cholesterol is partially obtained through the diet, while the majority is synthesized in the body, primarily in the liver. However, the limited exchange between the central nervous system and peripheral circulation, due to the presence of the blood-brain barrier, necessitates cholesterol in the brain to be exclusively acquired from local de novo synthesis. This cholesterol is reutilized efficiently, rendering a much slower overall turnover of the compound in the brain as compared with the periphery. Furthermore, brain cholesterol is regulated independently from peripheral cholesterol. Numerous enzymes, proteins, and other factors are involved in cholesterol synthesis and metabolism in the brain. Understanding the unique mechanisms and pathways involved in the maintenance of cholesterol homeostasis in the brain is critical, considering perturbations to these processes are implicated in numerous neurodegenerative diseases. This review focuses on the developing understanding of cholesterol metabolism in the brain, discussing the sites and processes involved in its synthesis and regulation, as well as the mechanisms involved in its distribution throughout, and elimination from, the brain.

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“…These data favor the hypothesis that 24S-OHC may be a good marker of "brain health" in old age, and would be increased during the progression of AD and decrease in later stages. As elevated concentrations of 24S-OHC induce cell death in neuronal cells [18,19], it has been suggested that 24S-OHC-induced lipotoxicity might contribute to neurodegeneration and brain atrophy. Among oxysterols, a variety of compounds that are derived from cholesterol autoxidation were also identified at increased levels in the frontal and occipital cortex.…”

Section: Mmentioning

confidence: 99%

“…with 7KC and 24S-OHC, and 158N and SK-N-BE cells treated with C24:0 [19,41,65,66,67]. In the heat inactivated FBS used the concentration of C24:0 was very low (682.20 nmol/L), and no 7KC and 24S-OHC were detected [68].…”

Section: Mmentioning

confidence: 99%

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)

et al. 2018

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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.

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Accumulation of 24S-hydroxycholesterol in neuronal SK-N-BE cells treated with hexacosanoic acid (C26:0): Argument in favor of 24S-hydroxycholesterol as a potential biomarker of neurolipotoxicity

Cited by 11 publications

References 22 publications

Tissue-Specific Oxysterols as Predictors of Antidepressant (Escitalopram) Treatment Response in Patients With Major Depressive Disorder

Tissue-Specific Oxysterols as Predictors of Antidepressant (Escitalopram) Treatment Response in Patients With Major Depressive Disorder

Balancing cholesterol in the brain: from synthesis to disposal

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)

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