dc.contributor.author | Sienel, RI | en_US |
dc.contributor.author | Mamrak, U | en_US |
dc.contributor.author | Biller, J | en_US |
dc.contributor.author | Roth, S | en_US |
dc.contributor.author | Zellner, A | en_US |
dc.contributor.author | Parakaw, T | en_US |
dc.contributor.author | Khambata, RS | en_US |
dc.contributor.author | Liesz, A | en_US |
dc.contributor.author | Haffner, C | en_US |
dc.contributor.author | Ahluwalia, A | en_US |
dc.contributor.author | Seker, BF | en_US |
dc.contributor.author | Plesnila, N | en_US |
dc.date.accessioned | 2023-12-20T12:00:45Z | |
dc.date.available | 2023-12-07 | en_US |
dc.date.issued | 2023-12-15 | en_US |
dc.identifier.uri | https://qmro.qmul.ac.uk/xmlui/handle/123456789/93163 | |
dc.description.abstract | Ischemic stroke is a major global health issue and characterized by acute vascular dysfunction and subsequent neuroinflammation. However, the relationship between these processes remains elusive. In the current study, we investigated whether alleviating vascular dysfunction by restoring vascular nitric oxide (NO) reduces post-stroke inflammation. Mice were subjected to experimental stroke and received inhaled NO (iNO; 50 ppm) after reperfusion. iNO normalized vascular cyclic guanosine monophosphate (cGMP) levels, reduced the elevated expression of intercellular adhesion molecule-1 (ICAM-1), and returned leukocyte adhesion to baseline levels. Reduction of vascular pathology significantly reduced the inflammatory cytokines interleukin-1β (Il-1β), interleukin-6 (Il-6), and tumor necrosis factor-α (TNF-α), within the brain parenchyma. These findings suggest that vascular dysfunction is responsible for leukocyte adhesion and that these processes drive parenchymal inflammation. Reversing vascular dysfunction may therefore emerge as a novel approach to diminish neuroinflammation after ischemic stroke and possibly other ischemic disorders. | en_US |
dc.format.extent | 301 - ? | en_US |
dc.language | eng | en_US |
dc.language.iso | en | en_US |
dc.relation.ispartof | J Neuroinflammation | en_US |
dc.rights | This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data. | |
dc.subject | Mice | en_US |
dc.subject | Animals | en_US |
dc.subject | Ischemic Stroke | en_US |
dc.subject | Nitric Oxide | en_US |
dc.subject | Neuroinflammatory Diseases | en_US |
dc.subject | Stroke | en_US |
dc.subject | Tumor Necrosis Factor-alpha | en_US |
dc.subject | Inflammation | en_US |
dc.subject | Intercellular Adhesion Molecule-1 | en_US |
dc.title | Inhaled nitric oxide suppresses neuroinflammation in experimental ischemic stroke. | en_US |
dc.type | Article | |
dc.rights.holder | Copyright © The Author(s) 2023 | |
dc.identifier.doi | 10.1186/s12974-023-02988-3 | en_US |
pubs.author-url | https://www.ncbi.nlm.nih.gov/pubmed/38102677 | en_US |
pubs.issue | 1 | en_US |
pubs.notes | Not known | en_US |
pubs.publication-status | Published online | en_US |
pubs.volume | 20 | en_US |
dcterms.dateAccepted | 2023-12-07 | en_US |
rioxxterms.funder | Default funder | en_US |
rioxxterms.identifier.project | Default project | en_US |