TY  - JOUR
A1  - Gatsiou, Aikaterini
A1  - Sopova, Kateryna
A1  - Tselepis, Alexandros
A1  - Stellos, Konstantinos L.
T1  - Interleukin-17A triggers the release of platelet-derived factors driving vascular endothelial cells toward a pro-angiogenic state
T2  - Cells
N2  - 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.
KW  - IL-17A
KW  - platelets
KW  - endothelial cells
KW  - angiogenesis
KW  - sprouting
KW  - VEGF
Y1  - 2021
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/62677
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-626773
SN  - 2073-4409
N1  - K. Stellos is supported by European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme (MODVASC, grant agreement No 759248) and the German Research Foundation DFG (SFB834 B12, project number 75732319). A.G. was supported for this work by the Hellenic Atherosclerosis Society and the European Union’s European Community Action Scheme for the Mobility of University Students (Erasmus programme). K. Sopova was supported by a research scholarship from the Deutsche Herzstiftung (German Heart Foundation).
VL  - 10
IS  - 8, art. 1855
SP  - 1
EP  - 15
PB  - MDPI
CY  - Basel
ER  -