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Gene expression profiling and pathway analysis of human bronchial epithelial cells exposed to airborne particulate matter collected from Saudi Arabia

机译:从沙特阿拉伯收集到空气中颗粒物质的人支气管上皮细胞的基因表达分析和途径分析

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摘要

Epidemiological studies have established a positive correlation between human mortality and increased concentration of airborne particulate matters (PM). However, the mechanisms underlying PM related human diseases, as well as the molecules and pathways mediating the cellular response to PM, are not fully understood. This study aims to investigate the global gene expression changes in human cells exposed to PM10 and to identify genes and pathways that may contribute to PM related adverse health effects. Human bronchial epithelial cells were exposed to PM10 collected from Saudi Arabia for 1 or 4 days, and whole transcript expression was profiled using the GeneChip human gene 1.0 ST array. A total of 140 and 230 genes were identified that significantly changed more than 1.5 fold after PM10 exposure for 1 or 4 days, respectively. Ingenuity Pathway Analysis revealed that different exposure durations triggered distinct pathways. Genes involved in NRF2-mediated response to oxidative stress were up-regulated after 1 day exposure. In contrast, cells exposed for 4 days exhibited significant changes in genes related to cholesterol and lipid synthesis pathways. These observed changes in cellular oxidative stress and lipid synthesis might contribute to PM related respiratory and cardiovascular disease.
机译:流行病学研究已建立了人类死亡率与空气中颗粒物(PM)浓度增加之间的正相关关系。然而,尚未完全了解与PM相关的人类疾病的潜在机制,以及介导细胞对PM应答的分子和途径。这项研究旨在调查暴露于PM10的人类细胞中全球基因表达的变化,并确定可能与PM相关的不良健康影响有关的基因和途径。将人支气管上皮细胞暴露于从沙特阿拉伯收集的PM10中1或4天,并使用GeneChip人基因1.0 ST阵列分析整个转录本的表达。总共鉴定出140和230个基因,分别在暴露PM10 1天或4天后发生了超过1.5倍的显着变化。创造力途径分析表明,不同的暴露时间触发了不同的途径。暴露1天后,涉及NRF2介导的对氧化应激反应的基因上调。相反,暴露4天的细胞在与胆固醇和脂质合成途径有关的基因中显示出显着变化。这些观察到的细胞氧化应激和脂质合成的变化可能导致与PM相关的呼吸道和心血管疾病。

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