Abstract
Occupational and environmental exposure to mercury is a public health concern worldwide. Although the altered epigenetic regulatory features, such as microRNA, have been associated with mercury exposure, the underlying molecular mechanism is not well illuminated. This study aimed to confirm that hsa-miR-92a and hsa-miR-486 are novel diagnostic biomarkers of occupational mercury poisoning, and to explore the underlying mechanism of miR-92a and miR-486 in mercury toxicity. RT-qPCR assays and receiver operating characteristics curve analyses were conducted to confirm the diagnostic value of miR-92a and miR-486 as biomarkers of occupational mercury poisoning. Dual-luciferase assay was applied to confirm the target gene of miR-92a and miR-486 in vitro. Then, we established an in-vitro model where miR-92a and miR-486 were overexpressed or knocked down in HEK-293 and HUVEC cells. RT-qPCR and western blotting were used to analyze gene and protein expression levels. Cell apoptosis was determined by flow cytometry. Results show that miR-92a and miR-486 expression levels were up-regulated in workers exposed to occupational mercury. Upregulation of miR-92a and miR-486 may play a crucial role in mercury toxicity by jointly activating the NF-κB signaling pathway via targeting KLF4 and Cezanne, respectively.
Highlights
Mercury (Hg) is one of the most widely used metals in industry, and is mainly used in mercury thermometer production and gold extraction
Subsequent experimental research revealed that exposure to mercury induced an increase in miR-92a and miR-486 expression, which led to increased nuclear factor-κB (NF-κB) and COX-2 activation and apoptosis of cells
NF-κB signaling plays a critical role in mediating the expression of numerous proinflammatory gene products, including COX-2 and inducible nitric oxide synthase, which are involved in inflammatory responses[17]
Summary
Mercury (Hg) is one of the most widely used metals in industry, and is mainly used in mercury thermometer production and gold extraction. The assumed mechanism of mercury toxicity mainly involves its ability of binding to sulfydryl containing enzyme, increasing oxidative stress and reducing oxidative defense[7]. These mechanisms cannot fully explain the damage to numerous organic systems that has been associated with mercury. Environmental and occupational toxicants such as mercury, lead and arsenic can alter epigenetic regulatory features such as DNA methylation, histone modification and microRNA (miRNA) expression pattern[8]. We identified plasma miRNAs hsa-miR-92a and hsa-miR-486 as potential markers to diagnose occupational mercury poisoning in workers[11]. We explore the underlying mechanism of miR-92a and miR-486 in mercury toxicity
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