Pentraxin 3 (PTX3), an acute-phase inflammation protein produced by several cell types, has long been described as a possible biomarker for age-related cardiovascular and cerebrovascular diseases. Although several mechanisms of action have been identified to date in the vascular and immune systems, the direct effects of PTX3 on isolated endothelial cells at morphological and metabolic levels remain unknown. PTX3 induced cytoplasmic vacuolization and dilution of mitochondrial matrix in isolated, human endothelial cells. Moreover, metabolic assays revealed that PTX3 increases respiratory capacity in support of mitochondrial function, and partially sustains the glycolytic pathway. PTX3 has, per se, a direct action on ultrastructural and bioenergetic parameters of isolated endothelial cells. This finding can be associated with our previous demonstration of a deleterious effect of PTX3 on the endothelial layer. More studies are needed to clearly demonstrate any direct correlation between these ultrastructural and bioenergetic changes with endothelial dysfunction, especially with regard to age-related cerebro- and cardio-vascular diseases.

中文翻译：

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PTX3：一种调节人内皮细胞超微结构和生物能量学的炎症蛋白

Pentraxin 3 (PTX3) 是一种由多种细胞类型产生的急性期炎症蛋白，长期以来一直被描述为与年龄相关的心血管和脑血管疾病的可能生物标志物。尽管迄今为止在血管和免疫系统中已经确定了几种作用机制，但 PTX3 在形态和代谢水平上对分离的内皮细胞的直接影响仍然未知。PTX3 在分离的人内皮细胞中诱导细胞质空泡化和线粒体基质稀释。此外，代谢测定显示 PTX3 增加呼吸能力以支持线粒体功能，并部分维持糖酵解途径。PTX3 本身对分离的内皮细胞的超微结构和生物能量参数具有直接作用。这一发现可能与我们先前证明 PTX3 对内皮层的有害影响有关。需要更多的研究来清楚地证明这些超微结构和生物能量变化与内皮功能障碍之间的任何直接相关性，特别是在与年龄相关的脑和心血管疾病方面。