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 α_IIbβ₃, 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 α_IIbβ₃ 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.

细胞外囊泡（EVs）是健康和疾病期间细胞通讯的介质，在激活或衰老过程中会被血小板大量释放。血小板电动汽车对免疫细胞和血管细胞发挥调节作用。血小板电动车可能会调节血管平滑肌细胞（SMC）的功能。从富含血小板的血浆中分离出血小板EV，并与SMC孵育，以评估细胞的结合，增殖，迁移和促炎表型。血小板电动汽车牢固地结合到通过血小板整α搁SMC _IIB β ₃，而在细胞因子刺激后，结合也以CX3CL1–CX3CR1依赖性方式发生。与血小板衍生的生长因子或血小板因子4相比，血小板EV增加SMC迁移，并诱导SMC增殖，这依赖于CD40和P选择素的相互作用。与静息SMC相比，增加了对血小板EV处理的SMC的耐流动性单核细胞粘附。再次，这种粘附依赖于整合素α _IIB β ₃和P-选择素，并在较小程度上作用于CD40和CX3CR1。用血小板电动车治疗SMC诱导白介素6分泌。最后，血小板电动车诱导合成的SMC形态并降低了钙蛋白的表达。总体而言，这些数据表明血小板电动汽车对SMC具有强大的免疫调节活性。尤其是，血小板电动车会引起向促炎表型的转换，从而刺激血管重塑。