Department of Physiology, China Pharmaceutical University, Nanjing, Jiangsu, China.
J Cardiovasc Pharmacol. 2012 Feb;59(2):124-32. doi: 10.1097/FJC.0b013e31820c6254.
Observational and experimental studies continue to support the association of infection and infection-stimulated inflammation with development of cardiovascular disease (CVD) including atherosclerosis and thrombosis. Microvesicles (MV) are heterogeneous populations of sealed membrane-derived vesicles shed into circulation by activated mammalian cells and/or pathogenic microbes that may represent an interface between bacterial/microbial infection and increased risk of CVD. This review evaluates how MV act to modulate and intersect immunological and inflammatory responses to infection with particular attention to progression of CVD. Although infection-related stimuli provoke release of MV from blood and vascular cells, MV express phosphatidylserine and other procoagulant factors on their surface, which initiate and amplify blood coagulation. In addition, MV mediate cell-cell adhesion, which may stimulate production of pro-inflammatory cytokines in vascular cells, which in turn aggravate progression of CVD and propagate atherothrombosis. MV transfer membrane receptors, RNA and proteins among cells, and present auto-antigens from their cells of origin to proximal or remote target cells. Because MV harbor cell surface proteins and contain cytoplasmic components of the parent cell, they mediate biological messages and play a pivotal role in the crossroad between infection-stimulated inflammation and CVDs.
观察性和实验性研究继续支持感染和感染引起的炎症与心血管疾病（CVD）包括动脉粥样硬化和血栓形成的发展之间的关联。微泡（MV）是由激活的哺乳动物细胞和/或致病微生物释放到循环中的封闭膜衍生囊泡的异质群体，它们可能代表细菌/微生物感染与 CVD 风险增加之间的接口。这篇综述评估了 MV 如何调节和交叉免疫和炎症反应，特别是 CVD 的进展。虽然与感染相关的刺激会促使 MV 从血液和血管细胞中释放出来，但 MV 表面表达磷脂酰丝氨酸和其他促凝因子，启动并放大血液凝固。此外，MV 介导细胞-细胞黏附，这可能刺激血管细胞中促炎细胞因子的产生，进而加重 CVD 的进展并促进动脉粥样血栓形成。MV 在细胞之间转移膜受体、RNA 和蛋白质，并将来自其起源细胞的自身抗原呈现给近端或远程靶细胞。由于 MV 含有细胞表面蛋白，并包含亲代细胞的细胞质成分，因此它们介导生物学信息，在感染刺激的炎症和 CVD 之间的交叉路口发挥关键作用。
