Identification of miRNAs induced by low-dose methylmercury exposure and their roles in inflammatory responses using human aortic endothelial cells
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Published on: June 17, 2015
Rika Matsuyama1, Athira Nandakumar1, Munekazu Yamakuchi2
1Department of Epidemiology and Preventive Medicine, Kagoshima University Graduate School of Medical and Dental Sciences.
Background:
Exposure to methylmercury (MeHg) is predominantly attributed to consumption of marine products. However, the general population is exposed to low MeHg levels, which can induce chronic inflammation. Although some MeHg-related microRNAs (miRNAs) have been reported, their functions remain elusive. The objective of this study was to identify the miRNAs induced by low-level MeHg exposure in a human endothelial cell line (HAECs). This study aimed to determine the specific miRNAs induced by low-level MeHg exposure using a HAECs as a potential novel and sensitive biomarker. The roles of miRNAs in inflammatory processes have been examined.
Methods:
Using HAECs, a miRNA microarray assay was performed to identify miRNAs with altered expression upon exposure to a non-cytotoxic MeHg level (0.1 and 1.5 µM). The expression patterns of interleukin-6 and -8, cyclooxygenase 2 (COX-2), RelB, and prostaglandin E2 (PGE2) were examined after transfection of the identified miRNAs with mimics/inhibitors.
Results:
Although the microarray assay identified six MeHg-specific miRNAs, miR-3613-5p, upregulated by 0.1 and 1.5 µM MeHg exposures, demonstrated the best reproducibility in HAECs. Transfection with the miR-3613-5p mimic enhanced the MeHg-induced inflammatory responses, including PGE2 and COX-2 protein levels, whereas the miR-3613-5p inhibitor suppressed these inflammatory responses.
Conclusion:
This study observed that miR-3613-5p is induced by low-dose MeHg exposure, plays a crucial role in the inflammatory process, and could serve as a novel and sensitive biomarker for low-level MeHg exposure.
Insights
Low-level methylmercury (MeHg) exposure induces miR-3613-5p in human endothelial cells, promoting inflammation. This microRNA shows potential as a sensitive biomarker for chronic MeHg exposure.
Area of Science:
- Environmental Toxicology
- Molecular Biology
- Biomarker Discovery
Background:
- Methylmercury (MeHg) exposure, primarily from seafood, can cause chronic inflammation even at low levels.
- MicroRNAs (miRNAs) are implicated in inflammatory processes, but their specific roles in MeHg toxicity are not fully understood.
- Human umbilical vein endothelial cells (HUVECs) are a relevant model for studying low-dose MeHg effects.
Purpose of the Study:
- To identify specific microRNAs (miRNAs) induced by low-level methylmercury (MeHg) exposure in human endothelial cells.
- To investigate the functional role of identified miRNAs in MeHg-induced inflammatory responses.
- To evaluate the potential of these miRNAs as sensitive biomarkers for low-dose MeHg exposure.
Main Methods:
- Human endothelial cells (HAECs) were exposed to non-cytotoxic levels of methylmercury (MeHg) (0.1 and 1.5 µM).
- MicroRNA microarray assays were performed to identify differentially expressed miRNAs.
- Expression of inflammatory markers (IL-6, IL-8, COX-2, PGE2) was analyzed following miRNA mimic or inhibitor transfections.
Main Results:
- Six MeHg-responsive miRNAs were identified, with miR-3613-5p showing consistent upregulation at both exposure levels.
- Overexpression of miR-3613-5p exacerbated MeHg-induced inflammatory responses, increasing PGE2 and COX-2 levels.
- Inhibition of miR-3613-5p suppressed these inflammatory markers, indicating its pro-inflammatory role.
Conclusions:
- miR-3613-5p is significantly induced by low-dose methylmercury (MeHg) exposure in human endothelial cells.
- This miRNA plays a critical role in mediating MeHg-induced inflammatory processes.
- miR-3613-5p represents a promising novel and sensitive biomarker for detecting low-level MeHg exposure.
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