dc.contributor.author |
Kim, Y |
en |
dc.contributor.author |
Davidson, Joanne |
en |
dc.contributor.author |
Gunn, KC |
en |
dc.contributor.author |
Phillips, Anthony |
en |
dc.contributor.author |
Green, Colin |
en |
dc.contributor.author |
Gunn, Alistair |
en |
dc.date.accessioned |
2016-04-22T02:12:52Z |
en |
dc.date.issued |
2016 |
en |
dc.identifier.citation |
Advances in Protein Chemistry and Structural Biology, 2016, 104 pp. 1 - 37 |
en |
dc.identifier.issn |
1876-1623 |
en |
dc.identifier.uri |
http://hdl.handle.net/2292/28637 |
en |
dc.description.abstract |
Neurodegenerative, cardiovascular, and metabolic disorders, once triggered, share a number of common features, including sustained inflammatory cell activation and vascular disruption. These shared pathways are induced independently of any genetic predisposition to the disease or the precise external stimulus. Glial cells respond to injury with an innate immune response that includes release of proinflammatory cytokines and chemokines. Vascular endothelial cells may also be affected, leading to opening of the blood-brain barrier that facilitates invasion by circulating inflammatory cells. Inflammation can trigger acute neural injury followed by chronic inflammation that plays a key role in neurodegenerative conditions. Gap junction channels normally allow direct cell-to-cell communication. They are formed by the docking of two hemichannels, one contributed by each of the neighboring cells. While the opening probability of these channels is tightly controlled under resting conditions, hemichannels can open in response to injury or inflammatory factors, forming a large, relatively nonselective membrane pore. In this review, we consider the CNS immune system from the perspective that modulating connexin hemichannel opening can prevent tissue damage arising from excessive and uncontrolled inflammation. We discuss connexin channel roles in microglia, astrocytes, and endothelial cells in both acute and chronic inflammatory conditions, and in particular describe the role of connexin hemichannels in the inflammasome pathway where they contribute to both its activation and its spread to neighboring cells. Finally, we describe the benefits of hemichannel block in animal models of brain injury. |
en |
dc.language |
English |
en |
dc.relation.ispartofseries |
Advances in Protein Chemistry and Structural Biology |
en |
dc.rights |
Items in ResearchSpace are protected by copyright, with all rights reserved, unless otherwise indicated. Previously published items are made available in accordance with the copyright policy of the publisher. Details obtained from http://www.sherpa.ac.uk/romeo/issn/1876-1623/
https://www.elsevier.com/about/company-information/policies/sharing |
en |
dc.rights.uri |
https://researchspace.auckland.ac.nz/docs/uoa-docs/rights.htm |
en |
dc.subject |
Connexin 43 |
en |
dc.subject |
Connexin hemichannels |
en |
dc.subject |
Cerebral ischemia |
en |
dc.subject |
Blood–brain barrier |
en |
dc.title |
Role of hemichannels in CNS inflammation and the inflammasome pathway |
en |
dc.type |
Journal Article |
en |
dc.identifier.doi |
10.1016/bs.apcsb.2015.12.001 |
en |
pubs.begin-page |
1 |
en |
pubs.volume |
104 |
en |
dc.identifier.pmid |
27038371 |
en |
pubs.author-url |
http://www.sciencedirect.com/science/article/pii/S187616231500098X |
en |
pubs.end-page |
37 |
en |
pubs.publication-status |
Published |
en |
dc.rights.accessrights |
http://purl.org/eprint/accessRights/RestrictedAccess |
en |
pubs.subtype |
Review |
en |
pubs.elements-id |
516747 |
en |
pubs.org-id |
Medical and Health Sciences |
en |
pubs.org-id |
Medical Sciences |
en |
pubs.org-id |
Physiology Division |
en |
pubs.org-id |
Science |
en |
pubs.org-id |
Biological Sciences |
en |
pubs.org-id |
Science Research |
en |
pubs.org-id |
Maurice Wilkins Centre (2010-2014) |
en |
dc.identifier.eissn |
1876-1631 |
en |
pubs.record-created-at-source-date |
2016-01-17 |
en |
pubs.dimensions-id |
27038371 |
en |