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Analysis of long non-coding RNA profiled following MC-LR-induced hepatotoxicity using high-throughput sequencing
Cong Wen1, Shu Yang1, Shuilin Zheng1
1a Department of Occupational and Environmental Health, Xiangya School of Public Health , Central South University , Changsha , Hunan , China.
Journal of Toxicology and Environmental Health. Part A
|November 16, 2018
Summary
Microcystin-LR (MC-LR), a liver toxin, alters long noncoding RNA (lncRNA) expression in human liver cells. Upregulation of LINC00847, MIR22HG, and LNC_00027 may contribute to MC-LR-induced liver damage.
Area of Science:
- Toxicology
- Molecular Biology
- Genomics
Background:
- Microcystin-LR (MC-LR) is a potent hepatotoxin posing global health risks.
- The molecular mechanisms of MC-LR-induced liver damage are not fully understood.
Purpose of the Study:
- To investigate the role of long noncoding RNAs (lncRNAs) in MC-LR-induced hepatotoxicity.
- To profile lncRNA expression changes in human liver cells after MC-LR exposure.
Main Methods:
- Human normal liver cell line (HL7702) treated with varying concentrations of MC-LR (1-10 μM).
- High-throughput sequencing to profile lncRNA expression.
- Quantitative real-time PCR (qPCR) for validation.
- Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses.
Main Results:
- Significant alterations in lncRNA expression observed across different MC-LR concentrations.
- LINC00847, MIR22HG, and the novel lncRNA LNC_00027 showed marked upregulation in all treatment groups.
- GO analysis indicated involvement in systems development, metabolism, and protein binding.
- KEGG analysis revealed upregulation of cancer, PI3K-AKT, and MAPK signaling pathways.
Conclusions:
- MC-LR exposure significantly alters lncRNA expression in human liver cells.
- Upregulated lncRNAs, including LINC00847, MIR22HG, and LNC_00027, may play crucial roles in MC-LR-mediated hepatotoxicity.
- These findings provide insights into the molecular mechanisms of MC-LR toxicity.
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