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Polychlorinated Biphenyl Exposure Alters tRNA Transcriptome in High-Fat Diet-Fed Mouse Liver
Carolyn M Klinge1,2, Julia H Chariker3,4, Kellianne M Piell1
1Department of Biochemistry and Molecular Genetics, University of Louisville School of Medicine, Louisville, KY 40202, USA.
Non-Coding RNA
|June 25, 2025
Summary
Polychlorinated biphenyls (PCBs) alter liver tRNA and tRNA-derived fragments (tRFs), impacting translation in mice exposed to high-fat diets. These findings reveal a novel role for PCBs in metabolic dysfunction-associated steatotic liver disease (MASLD) pathogenesis.
Area of Science:
- Environmental toxicology
- Molecular biology
- Hepatology
Background:
- High-fat diet (HFD) and polychlorinated biphenyls (PCBs) exposure induce metabolic dysfunction-associated steatotic liver disease (MASLD) and steatohepatitis (MASH).
- Mechanisms linking HFD, PCBs, and MASLD progression remain unclear.
- Previous studies identified altered tRNA modifications in HFD-fed mice after single PCB exposures.
Purpose of the Study:
- To investigate how PCB exposures impact the liver tRNA transcriptome, including tRNA-derived fragments (tRFs).
- To elucidate the role of specific PCBs (PCB126, Aroclor 1260) in altering tRNA expression and modifications.
Main Methods:
- Small RNA sequencing was employed to analyze liver samples from PCB-exposed mice.
- The tRNA analysis of expression (tRAX) pipeline was utilized to assess tRNA and tRF alterations.
- Specific PCB exposures included PCB126, Aroclor 1260 (Ar1260), and their combination.
Main Results:
- Distinct hepatic tRNA and tRF transcriptomes were observed for each PCB exposure, with more tRNAs decreased than increased.
- tRNA-Glu-TTC-1 was consistently reduced across all PCB exposure groups.
- Ar1260 exposure, alone or combined with PCB126, induced more tRF changes than PCB126 alone; four tRF-3s were upregulated with PCB126 co-exposure.
Conclusions:
- PCB exposures induce significant alterations in hepatic tRNAs and tRFs, suggesting a role in regulating liver translation.
- Specific tRF changes may be driven by PCB126, potentially through Angiogenin (ANG) pathway modulation.
- These findings highlight an unexplored mechanism by which PCBs contribute to liver disease pathogenesis.
