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首页> 外文期刊>Journal of applied toxicology >Water-soluble fraction of particulate matter < 2.5 mu m promoted lung epithelia cells apoptosis by regulating the expression of caveolin-1 and Kruppel-like factor 5
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Water-soluble fraction of particulate matter < 2.5 mu m promoted lung epithelia cells apoptosis by regulating the expression of caveolin-1 and Kruppel-like factor 5

机译：通过调节Caveolin-1和Kruppel样因子5的表达，颗粒物质的水溶性分数<2.5μm促进肺上皮细胞凋亡

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摘要

Ambient fine particulate matter of <2.5 mu m (PM2.5) has been linked to morbidity and mortality from respiratory and cardiovascular diseases. Lung epithelial cells bear the brunt of PM2.5 exposure. In the present study, we found that exposure of A549 cells to the water-soluble fraction of PM2.5 (WS-PM2.5) promoted the expression and internalization of caveolin-1. Caveolin-1 knockdown restrained the endocytosis of WS-PM2.5. In addition, WS-PM2.5 accumulation in the cells induced the phosphorylation of serine/threonine protein kinase B (AKT) and nuclear factor kappa-light-chain enhancer of activated B cells (NF kappa B), as well as the expression of Kruppel-like factor 5 (KLF5). Inhibiting activation of AKT and NF kappa B also partly reduced WS-PM2.5 concentration in cells, but KLF5 knockdown did not affect the intracellular accumulation of WS-PM2.5. KLF5 knockdown suppressed cytochrome P450 family 1 subfamily A member 1 (CYP1A1) expression and activated caspase 3. Luciferase reporter assay and chromatin immunoprecipitation assay showed that KLF5 positively regulated the transcription of KLF5. These results suggested that caveolin-1 was required for the endocytosis of WS-PM2.5. Intracellular accumulation of WS-PM2.5 activated AKT and NF kappa B, which facilitated WS-PM2.5 endocytosis. WS-PM2.5 accumulation also induced KLF5 expression, increasing the transcriptional expression of CYP1A1, which contributed to activate caspase 3.
机译：小于2.5μm的环境细颗粒物（PM2.5）与呼吸和心血管疾病的发病率和死亡率有关。肺上皮细胞首当其冲地受到PM2的影响。5.暴露。在本研究中，我们发现A549细胞暴露于PM2的水溶性部分。5（WS-PM2.5）促进小窝蛋白-1的表达和内化。Caveolin-1基因敲除抑制WS-PM2的内吞作用。5.此外，WS-PM2。5在细胞中的积累诱导丝氨酸/苏氨酸蛋白激酶B（AKT）和活化B细胞的核因子-κ轻链增强子（NF-κB）的磷酸化，以及Kruppel样因子5（KLF5）的表达。抑制AKT和NF-κB的激活也部分降低了WS-PM2。KLF5基因敲除不影响WS-PM2在细胞内的积累。5.KLF5基因敲除抑制细胞色素P450家族1亚家族A成员1（CYP1A1）的表达并激活半胱天冬酶3。荧光素酶报告试验和染色质免疫沉淀试验表明KLF5对KLF5的转录有正调控作用。这些结果表明，小窝蛋白-1是WS-PM2内吞所必需的。5.WS-PM2的细胞内积累。5激活AKT和NF-κB，促进WS-PM2。5内吞作用。WS-PM2。5积累还诱导KLF5表达，增加CYP1A1的转录表达，这有助于激活caspase 3。

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