The Role of Ion Channels Expressed in Cerebral Endothelial Cells in the Functional Integrity of the Blood-Brain Barrier (Review)

Shuvaev, Аnton N.; Кувачева, Н. В.; Моргун, А. В.; Хилажева, Е. Д.; Салмина, А. Б.

doi:10.17691/stm2016.8.4.29

Cited by 7 publications

(8 citation statements)

References 23 publications

(25 reference statements)

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“…When Cd is present in the blood stream, it can enter the cells by channels, transporters and receptors [124] that are present on the luminal surface of the BBB endothelial cells [125]. Once inside, Cd induces an oxidative stress response that in turn elicits an increase in the antioxidant enzymes' activity [104].…”

Section: Cadmium and Blood-brain Barriermentioning

confidence: 99%

Cadmium-Induced Oxidative Stress: Focus on the Central Nervous System

et al. 2020

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Cadmium (Cd), a category I human carcinogen, is a well-known widespread environmental pollutant. Chronic Cd exposure affects different organs and tissues, such as the central nervous system (CNS), and its deleterious effects can be linked to indirect reactive oxygen species (ROS) generation. Since Cd is predominantly present in +2 oxidation state, it can interplay with a plethora of channels and transporters in the cell membrane surface in order to enter the cells. Mitochondrial dysfunction, ROS production, glutathione depletion and lipid peroxidation are reviewed in order to better characterize the Cd-elicited molecular pathways. Furthermore, Cd effects on different CNS cell types have been highlighted to better elucidate its role in neurodegenerative disorders. Indeed, Cd can increase blood–brain barrier (BBB) permeability and promotes Cd entry that, in turn, stimulates pericytes in maintaining the BBB open. Once inside the CNS, Cd acts on glial cells (astrocytes, microglia, oligodendrocytes) triggering a pro-inflammatory cascade that accounts for the Cd deleterious effects and neurons inducing the destruction of synaptic branches.

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Section: Cadmium and Blood-brain Barriermentioning

confidence: 99%

Cadmium-Induced Oxidative Stress: Focus on the Central Nervous System

et al. 2020

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“…Direct influence of an increased BBB permeability on the EED dynamics is generation signals of the BBB via electrophysiological properties of brain endothelial cells forming the BBB. The signals generated by the BBB originate from a trans-endothelial voltage between blood and brain tissue This voltage is a consequence of unequal endothelial cell apical and basolateral membrane potentials [ 77 ]. The ion influx/efflux changes the BBB permeability via brain endothelial cells membrane depolarization affecting the cell stiffness via molecular mechanisms underlying cortical actin cytoskeleton [ 77 , 78 ].…”

Section: Slow Wave Activity As a Biomarker Of Disruption Of Blood-mentioning

confidence: 99%

“…The signals generated by the BBB originate from a trans-endothelial voltage between blood and brain tissue This voltage is a consequence of unequal endothelial cell apical and basolateral membrane potentials [ 77 ]. The ion influx/efflux changes the BBB permeability via brain endothelial cells membrane depolarization affecting the cell stiffness via molecular mechanisms underlying cortical actin cytoskeleton [ 77 , 78 ]. These changes of cell potential cause up to mV-level shifts in human scalp EEG [ 78 , 79 ].…”

Section: Slow Wave Activity As a Biomarker Of Disruption Of Blood-mentioning

confidence: 99%

Sleep as a Novel Biomarker and a Promising Therapeutic Target for Cerebral Small Vessel Disease: A Review Focusing on Alzheimer’s Disease and the Blood-Brain Barrier

Semyachkina-Glushkovskaya

Postnov

Penzel

et al. 2020

IJMS

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Cerebral small vessel disease (CSVD) is a leading cause of cognitive decline in elderly people and development of Alzheimer’s disease (AD). Blood–brain barrier (BBB) leakage is a key pathophysiological mechanism of amyloidal CSVD. Sleep plays a crucial role in keeping health of the central nervous system and in resistance to CSVD. The deficit of sleep contributes to accumulation of metabolites and toxins such as beta-amyloid in the brain and can lead to BBB disruption. Currently, sleep is considered as an important informative platform for diagnosis and therapy of AD. However, there are no effective methods for extracting of diagnostic information from sleep characteristics. In this review, we show strong evidence that slow wave activity (SWA) (0–0.5 Hz) during deep sleep reflects glymphatic pathology, the BBB leakage and memory deficit in AD. We also discuss that diagnostic and therapeutic targeting of SWA in AD might lead to be a novel era in effective therapy of AD. Moreover, we demonstrate that SWA can be pioneering non-invasive and bed–side technology for express diagnosis of the BBB permeability. Finally, we review the novel data about the methods of detection and enhancement of SWA that can be biomarker and a promising therapy of amyloidal CSVD and CSVD associated with the BBB disorders.

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“…However, blood–brain barrier (BBB) dysfunction is associated with neurodegenerative disorders [ 116 ]. A study has reported that cadmium can enter the cells by destroying the BBB, when cadmium is present in the bloodstream [ 117 ], which causes neurotoxicity. In this review, we will focus on the role of autophagy in cadmium-induced neurotoxicity.…”

Section: The Toxicity Of Cadmium Toward the Kidney Liver Bone And Brainmentioning

confidence: 99%

The Effect of Oxidative Stress-Induced Autophagy by Cadmium Exposure in Kidney, Liver, and Bone Damage, and Neurotoxicity

Yue

et al. 2022

IJMS

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Environmental and occupational exposure to cadmium has been shown to induce kidney damage, liver injury, neurodegenerative disease, and osteoporosis. However, the mechanism by which cadmium induces autophagy in these diseases remains unclear. Studies have shown that cadmium is an effective inducer of oxidative stress, DNA damage, ER stress, and autophagy, which are thought to be adaptive stress responses that allow cells exposed to cadmium to survive in an adverse environment. However, excessive stress will cause tissue damage by inducing apoptosis, pyroptosis, and ferroptosis. Evidently, oxidative stress-induced autophagy plays different roles in low- or high-dose cadmium exposure-induced cell damage, either causing apoptosis, pyroptosis, and ferroptosis or inducing cell survival. Meanwhile, different cell types have different sensitivities to cadmium, which ultimately determines the fate of the cell. In this review, we provided a detailed survey of the current literature on autophagy in cadmium-induced tissue damage. A better understanding of the complex regulation of cell death by autophagy might contribute to the development of novel preventive and therapeutic strategies to treat acute and chronic cadmium toxicity.

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The Role of Ion Channels Expressed in Cerebral Endothelial Cells in the Functional Integrity of the Blood-Brain Barrier (Review)

Cited by 7 publications

References 23 publications

Cadmium-Induced Oxidative Stress: Focus on the Central Nervous System

Cadmium-Induced Oxidative Stress: Focus on the Central Nervous System

Sleep as a Novel Biomarker and a Promising Therapeutic Target for Cerebral Small Vessel Disease: A Review Focusing on Alzheimer’s Disease and the Blood-Brain Barrier

The Effect of Oxidative Stress-Induced Autophagy by Cadmium Exposure in Kidney, Liver, and Bone Damage, and Neurotoxicity

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