Effects of transcranial direct current stimulation on hemichannel pannexin-1 and neural plasticity in rat model of cerebral infarction

Jiang, Tao; Xu, Ran; Zhang, A.W.; Di, Wei; Xiao, Zhupeng; Miao, Jia yin.; Luo, Ning-xiang; Yu, Fang

doi:10.1016/j.neuroscience.2012.09.035

Cited by 50 publications

(34 citation statements)

References 21 publications

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“…The depolarization in question does not occur until after about 10 min of continuous ischemic insult, and is reversible if normoxic conditions are reasserted soon after the drop in membrane resistance develops, but it becomes cytotoxic if allowed to persist for more than ~5 min. Panx1 channel blockers, siRNAs, and knockout all lessen damage following oxygen/glucose deprivation, thus supporting the hypothesis that Panx1 is indeed involved (Domercq et al, 2010; Bargiotas et al, 2011; Dvoriantchikova et al, 2012; Jiang et al, 2012). N-methyl-D-aspartate (NMDA) receptors could be the upstream cause of these destructive anoxic depolarization events, by regulating Panx1 permeability via Src family kinase mediated intracellular signaling (Weilinger et al, 2012).…”

Section: Pannexinssupporting

confidence: 55%

The pannexins: past and present

Bond

Naus

2014

Front. Physiol.

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The pannexins (Panxs) are a family of chordate proteins homologous to the invertebrate gap junction forming proteins named innexins. Three distinct Panx paralogs (Panx1, Panx2, and Panx3) are shared among the major vertebrate phyla, but they appear to have suppressed (or even lost) their ability to directly couple adjacent cells. Connecting the intracellular and extracellular compartments is now widely accepted as Panx's primary function, facilitating the passive movement of ions and small molecules along electrochemical gradients. The tissue distribution of the Panxs ranges from pervasive to very restricted, depending on the paralog, and are often cell type-specific and/or developmentally regulated within any given tissue. In recent years, Panxs have been implicated in an assortment of physiological and pathophysiological processes, particularly with respect to ATP signaling and inflammation, and they are now considered to be a major player in extracellular purinergic communication. The following is a comprehensive review of the Panx literature, exploring the historical events leading up to their discovery, outlining our current understanding of their biochemistry, and describing the importance of these proteins in health and disease.

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Section: Pannexinssupporting

confidence: 55%

The pannexins: past and present

Bond

Naus

2014

Front. Physiol.

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“…There are few studies that have investigated the transcriptional control of Panx1 and there is currently limited data on pathophysiological mechanisms controlling Panx1 expression (Boyce et al, 2018). Jiang et al reported increases in expression of Panx1 in mouse models of inducible stroke, which are associated with increased TNF-induced inflammation and tissue injury (Bokhari et al, 2014; Jiang et al, 2012; Liu and McCullough, 2011; Tuttolomondo et al, 2009; Tuttolomondo et al, 2014). In silico analysis has highlighted a number of transcriptional start sites within the rat Panx1 sequence, with binding sites for several transcription factors including CREB and ETV4 as well as factors downstream from IL-6 that have been identified (Dufresne and Cyr, 2014).…”

Section: Discussionmentioning

confidence: 99%

Endothelial pannexin 1 channels control inflammation by regulating intracellular calcium

Yang

DeLalio

Best

et al. 2019

Preprint

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25inflammation, endothelial cell, smooth muscle cell 4 to prolonged tumor necrosis factor alpha (TNF) treatment, Yang et al. found that the Panx1 5 channel is targeted to the plasma membrane, where it facilitates an increase in intracellular 6 calcium to control the production and release of cytokines including IL-1β. 7 8 GRAPHICAL ABSTRACT 9 10 Graphical Abstract: The inflammatory process in endothelial cells is controlled by Ca 2+ entry through Pannexin 1 membrane channels. 3 Abstract 1The proinflammatory cytokine IL-1β is a significant risk factor in cardiovascular disease 2 that can be targeted to reduce major cardiovascular events. IL-1β expression and release 3 are tightly controlled by changes in intracellular Ca 2+ . In addition, purinergic signaling 4 through ATP release has also been reported to promote IL-1β production. Despite this, 5 the mechanisms that control IL-1β synthesis and expression have not been identified. 6The pannexin 1 (Panx1) channel has canonically been implicated in ATP release, 7 especially during inflammation. However, resolution of purinergic signaling occurs quickly 8 due to blood flow and the presence of ectonucleotidases. We examined Panx1 in human 9 endothelial cells following treatment with the pro-inflammatory cytokine tumor necrosis 10 alpha (TNF). In response to long-term TNF treatment, we identified a dramatic increase 11 in Panx1 protein expression at the plasma membrane. Analysis by whole transcriptome 12 sequencing (RNA-seq), qPCR, and treatment with specific kinase inhibitors, revealed that 13 TNF signaling induced NFκβ-associated Panx1 transcription. Genetic inhibition of Panx1 14 reduced the expression and secretion of IL-1β. We initially hypothesized that increased 15Panx1-mediated ATP release acted in a paracrine fashion to control cytokine expression. 16However, our data demonstrate that IL1-β expression was not altered after direct ATP 17 stimulation, following degradation of ATP by apyrase, or after pharmacological blockade 18 of P2 receptors. These data suggest that non-purinergic pathways, involving Panx1, 19 control IL-1β production. Because Panx1 forms a large pore channel, we hypothesized it 20 may act to passively diffuse Ca 2+ into the cell upon opening to regulate IL-1β. High-21 throughput flow cytometric analysis demonstrated that TNF treatments lead to elevated 22 intracellular Ca 2+ . Genetic or pharmacological inhibition of Panx1 reduced TNF-23 associated increases in intracellular Ca 2+ , and IL-1β transcription. Furthermore, we found 24 that the Ca 2+ -sensitive NFκβ-p65 protein failed to localize to the nucleus after genetic or 25 pharmacological block of Panx1. Taken together, our study provides the first evidence 26 that intracellular Ca 2+ regulation via the Panx1 channel induces a feed-forward effect on 27NFκβ to regulate IL-1β synthesis and release in endothelium during inflammation. 28 4 (Tumor Necrosis Factor)-Triggered Smooth Muscle Cell Inflammation and Attenuates

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“…These neuronal growth-promoting proteins are overexpressed during dendritic remodeling and axonal regrowth throughout the acute phase of stroke [83,84]. Anodal stimulation also modulated pannexin-1 (PX1) hemichannel levels [85,86] and, following an ischemic insult, neurostimulation decreased rat PX1 mRNA and, consequently, augmented dendritic spine density in the surrounding areas of cerebral infarction; these cellular outcomes were associated with the improvement of motor function [85]. Some authors proposed that tDCS-induced improvement of stroke/TBI symptoms might be due to increase of BDNF expres-sion and associated with choline/creatine ratios in the perilesional cortex [31].…”

Section: Activation Of Neuroplasticity-associated Genementioning

confidence: 99%

Memory and Cognition-Related Neuroplasticity Enhancement by Transcranial Direct Current Stimulation in Rodents: A Systematic Review

2020

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Brain stimulation techniques, including transcranial direct current stimulation (tDCS), were identified as promising therapeutic tools to modulate synaptic plasticity abnormalities and minimize memory and learning deficits in many neuropsychiatric diseases. Here, we revised the effect of tDCS on the modulation of neuroplasticity and cognition in several animal disease models of brain diseases affecting plasticity and cognition. Studies included in this review were searched following the terms (“transcranial direct current stimulation”) AND (mice OR mouse OR animal) and according to the PRISMA statement requirements. Overall, the studies collected suggest that tDCS was able to modulate brain plasticity due to synaptic modifications within the stimulated area. Changes in plasticity-related mechanisms were achieved through induction of long-term potentiation (LTP) and upregulation of neuroplasticity-related proteins, such as c-fos, brain-derived neurotrophic factor (BDNF), or N-methyl-D-aspartate receptors (NMDARs). Taken into account all revised studies, tDCS is a safe, easy, and noninvasive brain stimulation technique, therapeutically reliable, and with promising potential to promote cognitive enhancement and neuroplasticity. Since the use of tDCS has increased as a novel therapeutic approach in humans, animal studies are important to better understand its mechanisms as well as to help improve the stimulation protocols and their potential role in different neuropathologies.

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Effects of transcranial direct current stimulation on hemichannel pannexin-1 and neural plasticity in rat model of cerebral infarction

Cited by 50 publications

References 21 publications

The pannexins: past and present

The pannexins: past and present

Endothelial pannexin 1 channels control inflammation by regulating intracellular calcium

Memory and Cognition-Related Neuroplasticity Enhancement by Transcranial Direct Current Stimulation in Rodents: A Systematic Review

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