Pannexin-1 Channels as Mediators of Neuroinflammation
Neuroinflammation is a major component of central nervous system (CNS) injuries and neurological diseases, including Alzheimer’s disease, multiple sclerosis, neuropathic pain, and brain trauma. The activation of innate immune cells at the damage site causes the release of pro-inflammatory cytokines...
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| Format: | Article |
| Language: | English |
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MDPI AG
2021-05-01
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| Series: | International Journal of Molecular Sciences |
| Subjects: | |
| Online Access: | https://www.mdpi.com/1422-0067/22/10/5189 |
| _version_ | 1797534199985471488 |
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| author | Joon Ho Seo Miloni S. Dalal Jorge E. Contreras |
| author_facet | Joon Ho Seo Miloni S. Dalal Jorge E. Contreras |
| author_sort | Joon Ho Seo |
| collection | DOAJ |
| description | Neuroinflammation is a major component of central nervous system (CNS) injuries and neurological diseases, including Alzheimer’s disease, multiple sclerosis, neuropathic pain, and brain trauma. The activation of innate immune cells at the damage site causes the release of pro-inflammatory cytokines and chemokines, which alter the functionality of nearby tissues and might mediate the recruitment of leukocytes to the injury site. If this process persists or is exacerbated, it prevents the adequate resolution of the inflammation, and ultimately enhances secondary damage. Adenosine 5′ triphosphate (ATP) is among the molecules released that trigger an inflammatory response, and it serves as a chemotactic and endogenous danger signal. Extracellular ATP activates multiple purinergic receptors (P2X and P2Y) that have been shown to promote neuroinflammation in a variety of CNS diseases. Recent studies have shown that Pannexin-1 (Panx1) channels are the principal conduits of ATP release from dying cells and innate immune cells in the brain. Herein, we review the emerging evidence that directly implicates Panx-1 channels in the neuroinflammatory response in the CNS. |
| first_indexed | 2024-03-10T11:26:16Z |
| format | Article |
| id | doaj.art-d5b2a8d00174460a8f52ed99709e6530 |
| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-10T11:26:16Z |
| publishDate | 2021-05-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | International Journal of Molecular Sciences |
| spelling | doaj.art-d5b2a8d00174460a8f52ed99709e65302023-11-21T19:40:58ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672021-05-012210518910.3390/ijms22105189Pannexin-1 Channels as Mediators of NeuroinflammationJoon Ho Seo0Miloni S. Dalal1Jorge E. Contreras2Department of Neurology and Nash Family, Department of Neuroscience, Friedman Brain Institute, Icahn School of Medicine, Mount Sinai, New York, NY 10029, USADepartment of Pharmacology, Physiology and Neuroscience, New Jersey Medical School, Rutgers University, Newark, NJ 07103, USADepartment of Pharmacology, Physiology and Neuroscience, New Jersey Medical School, Rutgers University, Newark, NJ 07103, USANeuroinflammation is a major component of central nervous system (CNS) injuries and neurological diseases, including Alzheimer’s disease, multiple sclerosis, neuropathic pain, and brain trauma. The activation of innate immune cells at the damage site causes the release of pro-inflammatory cytokines and chemokines, which alter the functionality of nearby tissues and might mediate the recruitment of leukocytes to the injury site. If this process persists or is exacerbated, it prevents the adequate resolution of the inflammation, and ultimately enhances secondary damage. Adenosine 5′ triphosphate (ATP) is among the molecules released that trigger an inflammatory response, and it serves as a chemotactic and endogenous danger signal. Extracellular ATP activates multiple purinergic receptors (P2X and P2Y) that have been shown to promote neuroinflammation in a variety of CNS diseases. Recent studies have shown that Pannexin-1 (Panx1) channels are the principal conduits of ATP release from dying cells and innate immune cells in the brain. Herein, we review the emerging evidence that directly implicates Panx-1 channels in the neuroinflammatory response in the CNS.https://www.mdpi.com/1422-0067/22/10/5189neuroinflammationPannexin-1hemichannelbrain injury |
| spellingShingle | Joon Ho Seo Miloni S. Dalal Jorge E. Contreras Pannexin-1 Channels as Mediators of Neuroinflammation International Journal of Molecular Sciences neuroinflammation Pannexin-1 hemichannel brain injury |
| title | Pannexin-1 Channels as Mediators of Neuroinflammation |
| title_full | Pannexin-1 Channels as Mediators of Neuroinflammation |
| title_fullStr | Pannexin-1 Channels as Mediators of Neuroinflammation |
| title_full_unstemmed | Pannexin-1 Channels as Mediators of Neuroinflammation |
| title_short | Pannexin-1 Channels as Mediators of Neuroinflammation |
| title_sort | pannexin 1 channels as mediators of neuroinflammation |
| topic | neuroinflammation Pannexin-1 hemichannel brain injury |
| url | https://www.mdpi.com/1422-0067/22/10/5189 |
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