Platelet extracellular vesicles induce a pro-inflammatory smooth muscle cell phenotype
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|Title:||Platelet extracellular vesicles induce a pro-inflammatory smooth muscle cell phenotype||Authors:||Vajen, Tanja
Heinzmann, Alexandra C. A.
Parsons, Martin E.M.
Maguire, Patricia B.
|Permanent link:||http://hdl.handle.net/10197/9956||Date:||16-May-2017||Online since:||2019-04-15T11:57:55Z||Abstract:||Extracellular vesicles (EVs) are mediators of cell communication during health and disease, and abundantly released by platelets upon activation or during ageing. Platelet EVs exert modulatory effects on immune and vascular cells. Platelet EVs may modulate the function of vascular smooth muscle cells (SMC). Platelet EVs were isolated from platelet-rich plasma and incubated with SMC in order to assess binding, proliferation, migration and pro-inflammatory phenotype of the cells. Platelet EVs firmly bound to resting SMC through the platelet integrin αIIbβ3, while binding also occurred in a CX3CL1–CX3CR1-dependent manner after cytokine stimulation. Platelet EVs increased SMC migration comparable to platelet derived growth factor or platelet factor 4 and induced SMC proliferation, which relied on CD40- and P-selectin interactions. Flow-resistant monocyte adhesion to platelet EV-treated SMC was increased compared with resting SMC. Again, this adhesion depended on integrin αIIbβ3 and P-selectin, and to a lesser extent on CD40 and CX3CR1. Treatment of SMC with platelet EVs induced interleukin 6 secretion. Finally, platelet EVs induced a synthetic SMC morphology and decreased calponin expression. Collectively, these data indicate that platelet EVs exert a strong immunomodulatory activity on SMC. In particular, platelet EVs induce a switch towards a pro-inflammatory phenotype, stimulating vascular remodelling.||Type of material:||Journal Article||Publisher:||Taylor & Francis||Journal:||Journal of Extracellular Vesicles||Volume:||6||Issue:||1||Copyright (published version):||2017 the Authors||Keywords:||Platelet factor 4; Cytokine; Synthetic phenotype; Vascular remodelling; Pathway analysis; Proteomics; CX3CR1||DOI:||10.1080/20013078.2017.1322454||Language:||en||Status of Item:||Peer reviewed|
|Appears in Collections:||Conway Institute Research Collection|
Biomolecular and Biomedical Science Research Collection
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