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DC Field | Value | Language |
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dc.contributor.author | Vital, SA | - |
dc.contributor.author | Senchenkova, EY | - |
dc.contributor.author | Ansari, J | - |
dc.contributor.author | Gavins, FNE | - |
dc.date.accessioned | 2021-02-05T17:10:10Z | - |
dc.date.available | 2020-11-13 | - |
dc.date.available | 2021-02-05T17:10:10Z | - |
dc.date.issued | 2020-11-13 | - |
dc.identifier.citation | Vital, S.A., Senchenkova, E.Y., Ansari, J. and Gavins, F.N.E. (2020) 'Targeting AnxA1/Formyl Peptide Receptor 2 Pathway Affords Protection against Pathological Thrombo-Inflammation', Cells, 9 (11). doi: 10.3390/cells9112473. | en_US |
dc.identifier.uri | https://bura.brunel.ac.uk/handle/2438/22186 | - |
dc.description.abstract | © 2020 by the authors. Stroke is a leading cause of death and disability globally and is associated with a number of co-morbidities including sepsis and sickle cell disease (SCD). Despite thrombo-inflammation underlying these co-morbidities, its pathogenesis remains complicated and drug discovery programs aimed at reducing and resolving the detrimental effects remain a major therapeutic challenge. The objective of this study was to assess whether the anti-inflammatory pro-resolving protein Annexin A1 (AnxA1) was able to reduce inflammation-induced thrombosis and suppress platelet activation and thrombus formation in the cerebral microvasculature. Using two distinct models of pathological thrombo-inflammation (lipopolysaccharide (LPS) and sickle transgenic mice (STM)), thrombosis was induced in the murine brain using photoactivation (light/dye) coupled with intravital microscopy. The heightened inflammation-induced microvascular thrombosis present in these two distinct thrombo-inflammatory models was inhibited significantly by the administration of AnxA1 mimetic peptide AnxA1Ac2-26 (an effect more pronounced in the SCD model vs. the endotoxin model) and mediated by the key resolution receptor, Fpr2/ALX. Furthermore, AnxA1Ac2-26 treatment was able to hamper platelet aggregation by reducing platelet stimulation and aggregation (by moderating αIIbβ3 and P-selectin). These findings suggest that targeting the AnxA1/Fpr2/ALX pathway represents an attractive novel treatment strategy for resolving thrombo-inflammation, counteracting e.g., stroke in high-risk patient cohorts. | en_US |
dc.description.sponsorship | The American Heart Association, grant number 16IRG27790071; Royal Society Wolfson Foundation, grant number RSWF\R3\183001 (FNEG). | en_US |
dc.language.iso | en_US | en_US |
dc.publisher | MDPI | en_US |
dc.rights | © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). | - |
dc.rights.uri | https://creativecommons.org/licenses/by/4.0/ | - |
dc.subject | thrombosis | en_US |
dc.subject | inflammation | en_US |
dc.subject | Annexin A1 | en_US |
dc.subject | formyl peptide receptors | en_US |
dc.subject | sickle cell disease | en_US |
dc.subject | sepsis | en_US |
dc.title | Targeting AnxA1/Formyl Peptide Receptor 2 Pathway Affords Protection against Pathological Thrombo-Inflammation | en_US |
dc.type | Article | en_US |
dc.identifier.doi | https://doi.org/10.3390/cells9112473 | - |
dc.relation.isPartOf | Cells | - |
pubs.issue | 11 | - |
pubs.publication-status | Published | - |
pubs.volume | 9 | - |
dc.identifier.eissn | 2073-4409 | - |
Appears in Collections: | Dept of Life Sciences Research Papers |
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