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Lookup NU author(s): Dr Aikaterini GatsiouORCiD, Dr Kateryna Sopova, Professor Konstantinos StellosORCiD
This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).
Platelets comprise a highly interactive immune cell subset of the circulatory system traditionally known for their unique haemostatic properties. Although platelets are considered as a vault of growth factors, cytokines and chemokines with pivotal role in vascular regeneration and angiogenesis, the exact mechanisms by which they influence vascular endothelial cells (ECs) function remain underappreciated. In the present study, we examined the role of human IL-17A/IL-17RA axis in platelet-mediated pro-angiogenic responses. We reveal that IL-17A receptor (IL-17RA) mRNA is present in platelets transcriptome and a profound increase is documented on the surface of activated platelets. By quantifying the protein levels of several factors, involved in angiogenesis, we identified that IL-17A/IL17RA axis selectively induces the release of vascular endothelial growth factor, interleukin -2 and -4, as well as monocyte chemoattractant protein -1 from treated platelets. However, IL-17A exerted no effect on the release of IL-10, an anti-inflammatory factor with potentially anti-angiogenic properties, from platelets. Treatment of human endothelial cell two-dimensional tubule networks or three-dimensional spheroid and mouse aortic ring structures with IL-17A-induced platelet releasate evoked pro-angiogenic responses of ECs. Our findings suggest that IL-17A may critically affect platelet release of pro-angiogenic factors driving ECs towards a pro-angiogenic state.
Author(s): Gatsiou A, Sopova K, Tselepis A, Stellos K
Publication type: Article
Publication status: Published
Journal: Cells
Year: 2021
Volume: 10
Issue: 8
Online publication date: 22/07/2021
Acceptance date: 20/07/2021
Date deposited: 01/10/2021
ISSN (electronic): 2073-4409
Publisher: MDPI
URL: https://doi.org/10.3390/cells10081855
DOI: 10.3390/cells10081855
PubMed id: 34440624
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