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Exposure to Heptachlorodibenzo-p-dioxin (HpCDD) Regulates microRNA Expression in Human Lung Fibroblasts
Collynn F Woeller1, Thomas H Thatcher, Juilee Thakar
1Department of Environmental Medicine (Dr Woeller, Dr Hopke, Dr Phipps, Dr Utell); Department of Medicine (Dr Thatcher, Dr Sime, Dr Utell); Microbiology and Immunology (Dr Thakar, Mr Cornwell, Dr Phipps), University of Rochester Medical Center, Rochester; Center for Air Resources Engineering and Science, Clarkson University, Potsdam (Dr Hopke), New York; Emory University, Atlanta, Georgia (Dr Smith, Dr Jones); Department of Preventive Medicine and Biostatistics, Uniformed Services University, Bethesda, Maryland (Dr Krahl, Dr Mallon).
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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