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Polystyrene microplastics impair trophoblast invasion in vitro and alter microRNA expression targeting the angiogenesis pathway
Summary
In a lab study, researchers exposed placental cells to tiny polystyrene microplastic particles (the kind found in everyday plastic products) and found that the particles stuck to the cells and disrupted their ability to properly embed into tissue, a process crucial for building a healthy placenta. The microplastics also threw off genetic signals that control blood vessel growth, hinting at a possible way plastics could interfere with pregnancy. Since microplastics have already been found in human blood and placentas, this early-stage research raises concerns worth investigating further, though more studies are needed to confirm these effects happen in real pregnancies.
The presence of microplastics (MPs) in human blood and placenta provides evidence of human exposure to MPs and their accumulation in biological tissues. Adequate trophoblast invasion is essential for normal placentation. However, the effects of MPs exposure on microRNA (miRNA) expression regulating angiogenesis during early placental development on trophoblast function remain poorly understood. In this study, the interaction of polystyrene microplastics (PS-MPs) with the HTR8/SVneo trophoblast cell line was investigated, with a particular focus on miRNA, gene, and protein expression associated with angiogenic and hypoxia-related pathways. Scanning electron microscopy (SEM) revealed PS-MPs adherence and accumulation on the cell membrane. PS-MPs significantly impaired trophoblast invasion and altered the expression of vascular endothelial growth factor (VEGF) and its receptors. Increased miRNA expression, known to regulate angiogenesis, suggests alterations in the transcriptome underlying the observed reduction in invasion. MiRNAs dysregulated in inadequate trophoblast invasion were significantly altered. Overall, PS-MP exposure impairs trophoblast invasion and altering trophoblast miRNA expression targeting VEGF, activating hypoxia mediators, thereby affecting early placental functions.