Neri Tommaso, Pergoli Laura, Petrini Silvia, Gravendonk Lotte, Balia Cristina, Scalise Valentina, Amoruso Angela, Pedrinelli Roberto, Paggiaro Pierluigi, Bollati Valentina, Celi Alessandro
Laboratory of Respiratory Cell Biology, Department of Surgical, Medical, Molecular Pathology and Critical Area and Azienda Ospedaliero-Universitaria Pisana, Università degli Studi di Pisa, Pisa, Italy.
EPIGET - Epidemiology, Epigenetics and Toxicology Lab, - Department of Clinical Sciences and Community Health, Università degli Studi di Milano, Milan, Italy.
Toxicol In Vitro. 2016 Apr;32:333-8. doi: 10.1016/j.tiv.2016.02.001. Epub 2016 Feb 10.
Particulate airborne pollution is associated with increased cardiopulmonary morbidity. Microparticles are extracellular vesicles shed by cells upon activation or apoptosis involved in physiological processes such as coagulation and inflammation, including airway inflammation. We investigated the hypothesis that particulate matter causes the shedding of microparticles by human mononuclear and endothelial cells. Cells, isolated from the blood and the umbilical cords of normal donors, were cultured in the presence of particulate from a standard reference. Microparticles were assessed in the supernatant as phosphatidylserine concentration. Microparticle-associated tissue factor was assessed by an one-stage clotting assay. Nanosight technology was used to evaluate microparticle size distribution. Particulate matter induces a dose- and time- dependent, rapid (1h) increase in microparticle generation in both cells. These microparticles express functional tissue factor. Particulate matter increases intracellular calcium concentration and phospholipase C inhibition reduces microparticle generation. Nanosight analysis confirmed that upon exposure to particulate matter both cells express particles with a size range consistent with the definition of microparticles (50-1000 nm). Exposure of mononuclear and endothelial cells to particulate matter upregulates the generation of microparticles at least partially mediated by calcium mobilization. This observation might provide a further link between airborne pollution and cardiopulmonary morbidity.
空气中的微粒污染与心肺疾病发病率增加有关。微粒是细胞在激活或凋亡时释放的细胞外囊泡，参与凝血和炎症等生理过程，包括气道炎症。我们研究了颗粒物导致人单核细胞和内皮细胞释放微粒的假说。从正常供体的血液和脐带中分离出的细胞，在标准参考颗粒物存在的情况下进行培养。通过磷脂酰丝氨酸浓度评估上清液中的微粒。通过一步凝血试验评估微粒相关组织因子。使用纳米可视技术评估微粒大小分布。颗粒物在两种细胞中均诱导微粒生成呈剂量和时间依赖性的快速（1小时）增加。这些微粒表达功能性组织因子。颗粒物增加细胞内钙浓度，磷脂酶C抑制可减少微粒生成。纳米可视分析证实，暴露于颗粒物后，两种细胞均表达大小范围与微粒定义（50 - 1000纳米）一致的颗粒。单核细胞和内皮细胞暴露于颗粒物会上调微粒生成，这至少部分由钙动员介导。这一观察结果可能为空气污染与心肺疾病发病率之间提供进一步的联系。
