超细粒子
胚胎干细胞
CXCL2型
银屑病
干细胞
CXCL1型
炎症
细胞生物学
材料科学
化学
纳米技术
趋化因子
免疫学
医学
生物
生物化学
基因
趋化因子受体
作者
Zhanwen Cheng,Xiaoxing Liang,Shaojun Liang,Nuoya Yin,Francesco Faiola
标识
DOI:10.1016/j.jes.2019.06.016
摘要
Air pollution has been linked to many health issues, including skin conditions, especially in children. Among all the atmospheric pollutants, ultrafine particles have been deemed very dangerous since they can readily penetrate the lungs and skin, and be absorbed into the bloodstream. Here, we employed a human embryonic stem cell (hESC)-based differentiation system towards keratinocytes, to test the effects of ultrafine carbon particles, which mimic ambient ultrafine particles, at environment related concentrations. We found that 10 ng/mL to 10 μg/mL ultrafine carbon particles down-regulated the expression of the pluripotency marker SOX2 in hESCs. Moreover, 1 μg/mL to 10 μg/mL carbon particle treatments disrupted the keratinocyte differentiation, and up-regulated inflammation- and psoriasis-related genes, such as IL-1β, IL-6, CXCL1, CXCL2, CXCL3, CCL20, CXCL8, and S100A7 and S100A9, respectively. Overall, our results provide a new insight into the potential developmental toxicity of atmospheric ultrafine particles.
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