The Key Laboratory of Geriatrics, Beijing Hospital & Beijing Institute of Geriatrics, Ministry of Health, Beijing 100730, China
Laboratory of Electron Microscopy, Peking University First Hospital, Beijing 100034, China.
Exp Biol Med (Maywood). 2015 Jul;240(7):876-83. doi: 10.1177/1535370214565076. Epub 2015 Jan 10.
Platelets are key players in fundamental processes of vascular biology, such as angiogenesis, tissue regeneration, and tumor metastasis. However, the underlying mechanisms remain unclear. In this study, some tumor vascular endothelial cells were positively stained by antiplatelet antibodies. Further investigation revealed that platelets were taken up by endothelial cells in vitro and in vivo. Human umbilical vascular endothelial cells were rendered apoptotic under conditions of serum deprivation. However, endothelial apoptosis was suppressed and cell viability was enhanced when platelets were added to the cultures. Endothelial survival was paralleled by an upregulation of phosphorylated Akt and p70 S6K. In conclusion, this study demonstrated that platelets can be phagocytosed by endothelial cells, and the phagocytosed platelets could suppress endothelial apoptosis and promote cell viability level. The mechanism underlying this process involves the activation of Akt signaling.
血小板是血管生物学基本过程中的关键参与者，如血管生成、组织再生和肿瘤转移。然而，其潜在机制尚不清楚。在这项研究中，一些肿瘤血管内皮细胞被抗血小板抗体阳性染色。进一步的研究表明，血小板在体外和体内被内皮细胞摄取。在血清剥夺的条件下，人脐血管内皮细胞发生凋亡。然而，当向培养物中添加血小板时，内皮细胞凋亡受到抑制，细胞活力增强。内皮细胞的存活与磷酸化 Akt 和 p70 S6K 的上调平行。总之，本研究表明血小板可以被内皮细胞吞噬，吞噬的血小板可以抑制内皮细胞凋亡并提高细胞活力水平。这个过程的机制涉及 Akt 信号的激活。
