dc.contributor.author |
Rustenhoven, Justin |
en |
dc.contributor.author |
Scotter, Emma |
en |
dc.contributor.author |
Jansson, Deidre |
en |
dc.contributor.author |
Kho, Dan |
en |
dc.contributor.author |
Oldfield, RL |
en |
dc.contributor.author |
Bergin, PS |
en |
dc.contributor.author |
Mee, EW |
en |
dc.contributor.author |
Faull, Richard |
en |
dc.contributor.author |
Curtis, Maurice |
en |
dc.contributor.author |
Graham, SE |
en |
dc.contributor.author |
Park, In |
en |
dc.contributor.author |
Dragunow, Michael |
en |
dc.date.accessioned |
2016-12-20T03:22:37Z |
en |
dc.date.available |
2015-06-01 |
en |
dc.date.issued |
2015-07-13 |
en |
dc.identifier.citation |
Scientific Reports, 13 July 2015, 5, Article number 12132 |
en |
dc.identifier.issn |
2045-2322 |
en |
dc.identifier.uri |
http://hdl.handle.net/2292/31457 |
en |
dc.description.abstract |
Neuroinflammation contributes to the pathogenesis of several neurological disorders and pericytes are implicated in brain inflammatory processes. Cellular inflammatory responses are orchestrated by transcription factors but information on transcriptional control in pericytes is lacking. Because the transcription factor CCAAT/enhancer binding protein delta (C/EBPδ) is induced in a number of inflammatory brain disorders, we sought to investigate its role in regulating pericyte immune responses. Our results reveal that C/EBPδ is induced in a concentration- and time-dependent fashion in human brain pericytes by interleukin-1β (IL-1β). To investigate the function of the induced C/EBPδ in pericytes we used siRNA to knockdown IL-1β-induced C/EBPδ expression. C/EBPδ knockdown enhanced IL-1β-induced production of intracellular adhesion molecule-1 (ICAM-1), interleukin-8, monocyte chemoattractant protein-1 (MCP-1) and IL-1β, whilst attenuating cyclooxygenase-2 and superoxide dismutase-2 gene expression. Altered ICAM-1 and MCP-1 protein expression were confirmed by cytometric bead array and immunocytochemistry. Our results show that knock-down of C/EBPδ expression in pericytes following immune stimulation increased chemokine and adhesion molecule expression, thus modifying the human brain pericyte inflammatory response. The induction of C/EBPδ following immune stimulation may act to limit infiltration of peripheral immune cells, thereby preventing further inflammatory responses in the brain. |
en |
dc.description.uri |
https://www.ncbi.nlm.nih.gov/pubmed/26166618 |
en |
dc.format.medium |
Electronic |
en |
dc.language |
English |
en |
dc.publisher |
Nature Publishing Group |
en |
dc.relation.ispartofseries |
Scientific Reports |
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/2045-2322/
http://www.nature.com/srep/journal-policies/editorial-policies |
en |
dc.rights.uri |
https://researchspace.auckland.ac.nz/docs/uoa-docs/rights.htm |
en |
dc.rights.uri |
https://creativecommons.org/licenses/by/4.0/ |
en |
dc.title |
An anti-inflammatory role for C/EBPδ in human brain pericytes |
en |
dc.type |
Journal Article |
en |
dc.identifier.doi |
10.1038/srep12132 |
en |
pubs.volume |
5 |
en |
dc.description.version |
VoR - Version of Record |
en |
dc.identifier.pmid |
26166618 |
en |
pubs.author-url |
http://www.nature.com/articles/srep12132 |
en |
pubs.publication-status |
Published |
en |
dc.rights.accessrights |
http://purl.org/eprint/accessRights/RestrictedAccess |
en |
pubs.subtype |
Article |
en |
pubs.elements-id |
491780 |
en |
pubs.org-id |
Medical and Health Sciences |
en |
pubs.org-id |
Medical Sciences |
en |
pubs.org-id |
Anatomy and Medical Imaging |
en |
pubs.org-id |
Pharmacology |
en |
pubs.org-id |
Science |
en |
pubs.org-id |
Biological Sciences |
en |
dc.identifier.eissn |
2045-2322 |
en |
pubs.number |
12132 |
en |
pubs.record-created-at-source-date |
2016-12-20 |
en |
pubs.online-publication-date |
2015-07-13 |
en |
pubs.dimensions-id |
26166618 |
en |