Exposure to Heptachlorodibenzo-p-dioxin (HpCDD) Regulates microRNA Expression in Human Lung Fibroblasts.

Q1 Medicine International Journal of Occupational and Environmental Medicine Pub Date : 2019-12-01 DOI:10.1097/JOM.0000000000001691

C. Woeller, T. Thatcher, J. Thakar, Adam B Cornwell, M. Smith, Dean P. Jones, P. Hopke, P. Sime, Pamela L Krahl, Timothy M Mallon, R. Phipps, M. Utell

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引用次数: 9

Abstract

OBJECTIVE Benzo(ghi)perylene (BghiP) and 1,2,3,4,6,7,8-Heptachlorodibenzo-p-dioxin (HpCDD) were elevated in serum from personnel deployed to sites with open burn pits. Here, we investigated the ability of BghiP and HpCDD to regulate microRNA (miRNA) expression through the aryl hydrocarbon receptor (AHR). METHODS Human lung fibroblasts (HLFs) were exposed to BghiP and HpCDD. AHR activity was measured by reporter assay and gene expression. Deployment related miRNA were measured by quantitative polymerase chain reaction. AHR expression was depleted using siRNA. RESULTS BghiP displayed weak AHR agonist activity. HpCDD induced AHR activity in a dose-dependent manner. Let-7d-5p, miR-103-3p, miR-107, and miR-144-3p levels were significantly altered by HpCDD. AHR knockdown attenuated these effects. CONCLUSIONS These studies reveal that miRNAs previously identified in sera from personnel deployed to sites with open burn pits are altered by HpCDD exposure in HLFs.

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暴露于七氯二苯并对二恶英(HpCDD)可调节人肺成纤维细胞中microRNA的表达。

目的探讨在露天烧伤坑工作人员血清中苯并(hi)苝(BghiP)和1,2,3,4,6,7,8-七氯二苯并-对二恶英(HpCDD)含量升高的情况。在这里，我们研究了bhip和HpCDD通过芳烃受体(AHR)调节microRNA (miRNA)表达的能力。方法将人肺成纤维细胞(HLFs)暴露于bhip和HpCDD。采用报告基因法和基因表达法测定AHR活性。采用定量聚合酶链反应检测部署相关miRNA。使用siRNA减少AHR的表达。结果bghip表现出较弱的AHR激动活性。HpCDD诱导AHR活性呈剂量依赖性。HpCDD显著改变了Let-7d-5p、miR-103-3p、miR-107和miR-144-3p水平。AHR的敲除减弱了这些影响。这些研究表明，先前在被部署到露天烧伤坑地点的人员血清中发现的mirna会因暴露于HpCDD而改变。

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