Potassium channels at the crossroads of neuroinflammation and myelination in experimental models of multiple sclerosis

ELBini, Ines; Neili, Nour-elhouda

doi:10.1016/j.bbrc.2023.02.066

Cited by 4 publications

(2 citation statements)

References 48 publications

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“…Considering that in demyelinated pathologies, the myelin sheath breaks down, and MBP and its fragments are secreted into the extracellular fluid, we hypothesized that the action of MBP could play a significant role in oligodendrocyte–astrocyte interactions. Several studies have highlighted the cross-talk between astrocytes and oligodendrocytes ( ELBini and Neili, 2023 ). Three binding partners can interact with MBP in astrocytes: bFGF, LRP, and PRRs.…”

Section: Discussionmentioning

confidence: 99%

Citrullinated isomer of myelin basic protein can induce inflammatory responses in astrocytes

Chikviladze,

Mamulashvili,

Sepashvili

et al. 2024

IBRO Neuroscience Reports

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Section: Discussionmentioning

confidence: 99%

Citrullinated isomer of myelin basic protein can induce inflammatory responses in astrocytes

Chikviladze,

Mamulashvili,

Sepashvili

et al. 2024

IBRO Neuroscience Reports

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“…These findings suggest the development of a neuroinflammatory process in the sciatic nerve with Cuprizone feeding. Recently, ELBini and Neili [32] demonstrated that the use of a K channel blocker stimulated the process of the myelination of nerve fibers in a model of multiple sclerosis when introduced early during disease development or during remission and exacerbated the demyelination when introduced in a toxic inflammatory environment during the inflammatory processes. Moreover, vanillic acid treatment significantly decreased these inflammatory markers (IL-17, INF-γ) in the sciatic nerve, which is in parallel with the results of Katary & Salahuddin, [33] that vanillic acid downregulates inflammatory cytokines induced by indomethacin in the gastric mucosa.…”

Section: Discussionmentioning

confidence: 99%

Vanillic Acid Ameliorates Demyelination in a Cuprizone-Induced Multiple Sclerosis Rat Model: Possible Underlying Mechanisms

Safwat,

El Tohamy,

Aboonq

et al. 2023

Brain Sciences

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Objective: To investigate the effect of vanillic acid (VA) on a Cuprizone (Cup) demyelinating rat model and the mechanisms behind such effect. Methods: Thirty adult male Sprague Dawley (SD) rats were randomly divided into three groups: control, Cuprizone, and VA groups. Cuprizone was administrated at a dose of 450 mg/kg per day orally via gastric gavage for 5 weeks. The nerve conduction velocity (NCV) was studied in an isolated sciatic nerve, and then the sciatic nerve was isolated for histopathological examination, electron microscope examination, immunohistochemical staining, and biochemical and PCR assay. The level of IL17 was detected using ELISA, while the antioxidant genes Nrf2, HO-1 expression at the level of mRNA, expression of the myelin basic protein (MBP), interferon-gamma factor (INF)-γ and tumor necrosis factor (TNF)-α, and apoptotic marker (caspase-3) were measured using immunohistochemistry in the sciatic nerve. Results: There was a significant reduction in NCV in Cup compared to normal rats (p < 0.001), which was markedly improved in the VA group (p < 0.001). EM and histopathological examination revealed significant demyelination and deterioration of the sciatic nerve fibers with significant improvement in the VA group. The level of IL17 as well as the expression of INF-γ and caspase-3 were significantly increased with a significant reduction in the expression of MBP, Nrf2, and HO-1 in the sciatic nerve (p < 0.01), and VA treatment significantly improved the studied parameters (p < 0.01). Conclusion: The current study demonstrated a neuroprotective effect for VA against the Cup-induced demyelinating rat model. This effect might be precipitated by the inhibition of inflammation, oxidative stress, and apoptosis.

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Dysfunctional K+ Homeostasis as a Driver for Brain Inflammation

Ozsoy,

Dallas

2024

Encyclopedia

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The central nervous system (CNS) relies on precise regulation of potassium ion (K+) concentrations to maintain physiology. This regulation involves complex cellular and molecular mechanisms that work in concert to regulate both intracellular and extracellular K+ levels. Inflammation, a key physiological response, encompasses a series of cell-specific events leading to inflammasome activation. Perturbations in K+-sensitive processes can result in either chronic or uncontrolled inflammation, highlighting the intricate relationship between K+ homeostasis and inflammatory signalling. This review explores molecular targets that influence K+ homeostasis and have been implicated in inflammatory cascades, offering potential therapeutic avenues for managing inflammation. We examine both cell-specific and common molecular targets across different cell types, providing a comprehensive overview of the interplay between K+ regulation and inflammation in the CNS. By elucidating these mechanisms, we identify leads for drug discovery programmes aimed at modulating inflammatory responses. Additionally, we highlight potential consequences of targeting individual molecular entities for therapeutic purposes, emphasizing the need for a nuanced approach in developing anti-inflammatory strategies. This review considers current knowledge on K+-sensitive inflammatory processes within the CNS, offering critical insights into the molecular underpinnings of inflammation and potential therapeutic interventions. Our findings underscore the importance of considering K+ homeostasis in the development of targeted therapies for inflammatory conditions within the CNS.

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Potassium channels at the crossroads of neuroinflammation and myelination in experimental models of multiple sclerosis

Cited by 4 publications

References 48 publications

Citrullinated isomer of myelin basic protein can induce inflammatory responses in astrocytes

Citrullinated isomer of myelin basic protein can induce inflammatory responses in astrocytes

Vanillic Acid Ameliorates Demyelination in a Cuprizone-Induced Multiple Sclerosis Rat Model: Possible Underlying Mechanisms

Dysfunctional K+ Homeostasis as a Driver for Brain Inflammation

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