Correction: Contribution of Pannexin1 to Experimental Autoimmune Encephalomyelitis

Lutz, Sarah E.; González-Fernández, Estíbaliz; Ventura, Juan Carlos Chara; Pérez-Samartı́n, Alberto; Tarassishin, Leonid; Negoro, Hiromitsu; Patel, Naman K.; Suadicani, Sylvia O.; Lee, Sunhee C.; Matute, Carlos; Scemes, Eliana

doi:10.1371/annotation/cedbee08-9c0e-42e3-862f-df7409c273ef

Cited by 12 publications

(6 citation statements)

References 41 publications

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“…BBG decreased astrogliosis in the forebrain of immunized rats and alleviated the neurological symptoms. In view of the reported preferential localization of Panx-1 channels in astrocytes and their confirmed role in the release of the potentially neurotoxic ATP [145], it was interesting to observe that Panx-1 KO mice displayed a delayed onset of clinical signs of EAE and decreased mortality compared to wt mice [205].…”

Section: Multiple Sclerosis (Ms)mentioning

confidence: 99%

P2X7 Receptors Amplify CNS Damage in Neurodegenerative Diseases

Illéš

2020

IJMS

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ATP is a (co)transmitter and signaling molecule in the CNS. It acts at a multitude of ligand-gated cationic channels termed P2X to induce rapid depolarization of the cell membrane. Within this receptor-channel family, the P2X7 receptor (R) allows the transmembrane fluxes of Na+, Ca2+, and K+, but also allows the slow permeation of larger organic molecules. This is supposed to cause necrosis by excessive Ca2+ influx, as well as depletion of intracellular ions and metabolites. Cell death may also occur by apoptosis due to the activation of the caspase enzymatic cascade. Because P2X7Rs are localized in the CNS preferentially on microglia, but also at a lower density on neuroglia (astrocytes, oligodendrocytes) the stimulation of this receptor leads to the release of neurodegeneration-inducing bioactive molecules such as pro-inflammatory cytokines, chemokines, proteases, reactive oxygen and nitrogen molecules, and the excitotoxic glutamate/ATP. Various neurodegenerative reactions of the brain/spinal cord following acute harmful events (mechanical CNS damage, ischemia, status epilepticus) or chronic neurodegenerative diseases (neuropathic pain, Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, amyotrophic lateral sclerosis) lead to a massive release of ATP via the leaky plasma membrane of neural tissue. This causes cellular damage superimposed on the original consequences of neurodegeneration. Hence, blood-brain-barrier permeable pharmacological antagonists of P2X7Rs with excellent bioavailability are possible therapeutic agents for these diseases. The aim of this review article is to summarize our present state of knowledge on the involvement of P2X7R-mediated events in neurodegenerative illnesses endangering especially the life quality and duration of the aged human population.

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Section: Multiple Sclerosis (Ms)mentioning

confidence: 99%

P2X7 Receptors Amplify CNS Damage in Neurodegenerative Diseases

Illéš

2020

IJMS

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“…This increase in receptor expression likely compensates for the decrease in ATP release observed in Panx1 KO mice and contributes to the development of EAE symptoms in these mice. This study demonstrates that a Panx1dependent mechanism involving ATP release and/or inflammasome activation plays a role in disease progression, and inhibiting Panx1 through pharmacological means or genetic disruption delays and mitigates the clinical signs of EAE [41].…”

Section: Eae In Pannexin1 Deficient Micementioning

confidence: 74%

“…In the CNS, Panx1 is found in neurons and glial cells, and in the immune system, it is present in macrophages and T cells [40]. Lutz et al conducted a study to test the hypothesis that Panx1-mediated ATP release contributes to the development of EAE, using both wild-type (WT) and Panx1 KO mice [41]. The results showed that Panx1 KO mice exhibited a delayed onset of clinical signs of EAE and a reduced mortality rate compared to WT mice, although they developed comparable clinical severities to the WT mice.…”

Section: Eae In Pannexin1 Deficient Micementioning

confidence: 99%

Connexins Control Glial Inflammation in Various Neurological Diseases

Yamasaki

2023

IJMS

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Connexins (Cxs) form gap junctions through homotypic/heterotypic oligomerization. Cxs are initially synthesized in the endoplasmic reticulum, then assembled as hexamers in the Golgi apparatus before being integrated into the cell membrane as hemichannels. These hemichannels remain closed until they combine to create gap junctions, directly connecting neighboring cells. Changes in the intracellular or extracellular environment are believed to trigger the opening of hemichannels, creating a passage between the inside and outside of the cell. The size of the channel pore depends on the Cx isoform and cellular context-specific effects such as posttranslational modifications. Hemichannels allow various bioactive molecules, under ~1 kDa, to move in and out of the host cell in the direction of the electrochemical gradient. In this review, we explore the fundamental roles of Cxs and their clinical implications in various neurological dysfunctions, including hereditary diseases, ischemic brain disorders, degenerative conditions, demyelinating disorders, and psychiatric illnesses. The influence of Cxs on the pathomechanisms of different neurological disorders varies depending on the circumstances. Hemichannels are hypothesized to contribute to proinflammatory effects by releasing ATP, adenosine, glutamate, and other bioactive molecules, leading to neuroglial inflammation. Modulating Cxs’ hemichannels has emerged as a promising therapeutic approach.

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“…Cdc42. ITGB2, SRF and ERM family (ezrin/radixin/moesin) [46][47][48][49] (iv) Genes that enhance immune cells infiltration of endothelial cells in both paracellular and transcellular routes such as Panx1 [50,51]. (v) Genes that play different roles in paracellular and transcellular routes and these genes include LSP1 which is an endothelial F-actin binding protein, and it moves from the nucleus to the cytosol and is associated with the cytoskeleton on stimulation and the formation of the dome structures [52].…”

Section: Resultsmentioning

confidence: 99%

Paracellular and Transcellular Leukocytes Diapedesis Are Divergent but Interconnected Evolutionary Events

Mickael

Kubick

Klimovich³

et al. 2021

Genes

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Infiltration of the endothelial layer of the blood-brain barrier by leukocytes plays a critical role in health and disease. When passing through the endothelial layer during the diapedesis process lymphocytes can either follow a paracellular route or a transcellular one. There is a debate whether these two processes constitute one mechanism, or they form two evolutionary distinct migration pathways. We used artificial intelligence, phylogenetic analysis, HH search, ancestor sequence reconstruction to investigate further this intriguing question. We found that the two systems share several ancient components, such as RhoA protein that plays a critical role in controlling actin movement in both mechanisms. However, some of the key components differ between these two transmigration processes. CAV1 genes emerged during Trichoplax adhaerens, and it was only reported in transcellular process. Paracellular process is dependent on PECAM1. PECAM1 emerged from FASL5 during Zebrafish divergence. Lastly, both systems employ late divergent genes such as ICAM1 and VECAM1. Taken together, our results suggest that these two systems constitute two different mechanical sensing mechanisms of immune cell infiltrations of the brain, yet these two systems are connected. We postulate that the mechanical properties of the cellular polarity is the main driving force determining the migration pathway. Our analysis indicates that both systems coevolved with immune cells, evolving to a higher level of complexity in association with the evolution of the immune system.

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Correction: Contribution of Pannexin1 to Experimental Autoimmune Encephalomyelitis

Cited by 12 publications

References 41 publications

P2X7 Receptors Amplify CNS Damage in Neurodegenerative Diseases

P2X7 Receptors Amplify CNS Damage in Neurodegenerative Diseases

Connexins Control Glial Inflammation in Various Neurological Diseases

Paracellular and Transcellular Leukocytes Diapedesis Are Divergent but Interconnected Evolutionary Events

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