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The miR-122/P53/TIGAR signaling axis regulates glucose metabolic reprogramming induced by polystyrene nanoplastic particles
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Researchers identified a molecular pathway by which polystyrene nanoplastics disrupt glucose metabolism in zebrafish and liver cells: the particles suppress the liver-specific microRNA miR-122, which elevates the tumor suppressor p53 and its downstream effector TIGAR, rerouting energy production away from glycolysis and toward the pentose phosphate pathway.
Polystyrene nanoplastics (PS-NPs) are widespread environmental pollutants that cause toxicity, including metabolic disruption. However, their exact molecular mechanisms remain unclear. This study systematically investigated the effects of PS-NPs on glucose metabolism using both in vivo and in vitro models, employing zebrafish larvae and Hep G2 cell lines. It was found that exposure to PS-NPs induced oxidative stress and liver damage in zebrafish larvae, while the liver-specific expression of miR-122 was significantly downregulated, leading to the upregulation of its target gene P53 and its downstream effector TIGAR. Combined metabolomics and transcriptomics analysis showed that PS-NPs exposure caused glucose metabolism disorders, with P53 and its downstream effector TIGAR playing a key regulatory role in the glycolytic pathway (EMP) and the pentose phosphate pathway (PPP). Through miR-122-5p mimic, miR-122-5p inhibitor, P53 RNA interference, and co-transfection experiments, we further demonstrated that glucose metabolism could be driven from the EMP shifted to the PPP through the miR-122/P53/TIGAR axis. This study, for the first time, reveals the molecular mechanism by which PS-NPs regulate glucose metabolism via the miR-122/P53/TIGAR signaling axis. It provides a novel insight for understanding the impact of miR-122-mediated glucose metabolic reprogramming, and enhances the understanding of miRNA function in response to NPs exposure.
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