Phagocytosis of platelets enhances endothelial cell survival under serum deprivation
Phagocytosis of platelets enhances endothelial cell survival under serum deprivation
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血小板的吞噬作用增强血清剥夺条件下内皮细胞的存活
DOI：
10.1177/1535370214565076
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发表时间：
2015-07-01
影响因子：
3.2
通讯作者：
Cai, Jian-Ping
中科院分区：
文献类型：
--
作者：
Jiang, Ping;Ren, Ya-Li;Cai, Jian-Ping
血小板是血管生物学的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，其潜在机制仍不清楚。本研究中，部分肿瘤血管内皮细胞抗血小板抗体染色阳性。进一步的研究表明，血小板在体外和体内被内皮细胞摄取。人脐静脉内皮细胞在血清剥夺条件下发生凋亡。然而，内皮细胞凋亡被抑制，细胞活力增强时，血小板被添加到文化。磷酸化Akt和p70 S6K的上调会降低内皮细胞的存活率。本研究表明，血小板可以被内皮细胞吞噬，吞噬后的血小板可以抑制内皮细胞凋亡，提高细胞活力。该过程的潜在机制涉及Akt信号传导的激活。
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.