PDF(Pubmed)
Abstract：
Exposure to particulate matter ≤ 2.5 µm (PM2.5) is a risk factor for many lung diseases. Although the toxicologic effects of PM2.5 on airway epithelium are well-described, the effects of PM2.5 on fibroblasts in the lung are less studied. Here, we sought to examine the effects of PM2.5 on the differentiation of fibroblasts into myofibroblasts. Although a single treatment of fibroblasts did not result in a change in collagen or the myofibroblast marker α-SMA, exposing fibroblasts to sequential treatments with PM2.5 at low concentrations caused a robust increase in these proteins. Treatment of fibroblasts with IMD0354, an inhibitor to nuclear factor κB, but not with an antagonist to aryl hydrocarbon receptor, abolished the ability of PM2.5 to induce myofibroblast differentiation. These data demonstrate that potential impact of PM2.5 to fibroblast activation and fibrosis and support the importance of utilizing low concentrations and varying exposure protocols to toxicologic studies.
摘要：
暴露于颗粒物≤2.5μm（PM2.5）是许多肺部疾病的危险因素。尽管PM2.5对气道上皮的毒理学影响已得到很好的描述，PM2.5对肺成纤维细胞的影响研究较少。这里,我们试图研究PM2.5对成纤维细胞分化为肌成纤维细胞的影响.尽管成纤维细胞的单一处理不会导致胶原蛋白或肌成纤维细胞标志物α-SMA的变化，将成纤维细胞暴露于低浓度PM2.5的连续治疗会导致这些蛋白质的强劲增加。用核因子κB的抑制剂IMD0354治疗成纤维细胞，但不是用芳香烃受体的拮抗剂，消除了PM2.5诱导肌成纤维细胞分化的能力。这些数据表明PM2.5对成纤维细胞活化和纤维化的潜在影响，并支持利用低浓度和不同暴露方案进行毒理学研究的重要性。
