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颗粒物与基质的协同效应上皮-间充质转变的硬度Synergistic Effects of Particulate Matter and Substrate

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更新时间：2021-09-25
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燃烧源暴露于颗粒物（PM）与肺部炎症和损伤有关，这会触发修复反应以恢复正常的组织功能。随着时间的流逝，这些反应的调节异常会导致纤维化改变，其特征是成纤维细胞和成肌纤维细胞的数量增加以及胶原蛋白和纤连蛋白在细胞外基质中的异常沉积，从而导致基质硬度增加和气体交换障碍。一种理论认为成纤维细胞源自分化为间充质细胞的肺泡上皮细胞。该过程称为上皮-间充质转化（EMT）。与特发性纤维化一样，肺部纤维化可能是进行性和致命性的，也是慢性肺部疾病（例如哮喘）的特征，因此了解纤维化过程非常重要。在当前的研究中，曾获得HEI的Walter A. Rosenblith新研究者奖的Thomas H. Barker博士及其同事对以下假设进行了检验：生长在纤连蛋白底物上的刚度增加的肺泡上皮细胞会经历EMT，并且添加精细的PM（空气动力学直径为PM＃2.5 m [PM2.5]）将增强这些效果。

Exposure to particulate matter (PM) from combustion sources has been associated with lung inflammation and injury, which trigger repair responses to restore normal tissue function. Dysregulation of these responses can result, over time, in fibrotic changes characterized by increased numbers of fibroblasts and myofibroblasts and abnormal deposition of collagen and fibronectin in the extracellular matrix, with consequent increases in matrix stiffness and impairment of gas exchange. One theory proposes that the fibroblasts are derived from alveolar epithelial cells that differentiate into mesenchymal cells. This process is referred to as epithelial-to-mesenchymal transition (EMT). Fibrosis in the lung can be progressive and fatal, as in idiopathic fibrosis, and is also a feature of chronic pulmonary diseases such as asthma, and it is thus important to understand profibrotic processes. In the current study Dr. Thomas H. Barker, who was a recipient of HEI’s Walter A. Rosenblith New Investigator Award, and his colleagues tested the hypotheses that alveolar epithelial cells grown on fibronectin substrates of increasing stiffness would undergo EMT and that the addition of fine PM (PM # 2.5 m in aerodynamic diameter [PM2.5]) would enhance these effects.

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颗粒物与基质的协同效应上皮-间充质转变的硬度Synergistic Effects of Particulate Matter and Substrate

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