Transcriptomic and functional profiling of endothelial dysfunction induced by polystyrene nanoplastics

Additionally, RNA sequencing provided transcriptomic insights into the cellular response to PS-C-NPLs, complementing the in vitro findings and revealing molecular pathways underlying the observed effects. All three PS-C-NPL sizes were rapidly internalised by HUVECs within 20 minutes, inducing significant alterations in cell morphology, internal complexity, and function. PS-C-NPLs caused genotoxic damage and disrupted cholesterol metabolism, migration, angiogenesis, and inflammatory responses.

Notably, some effects exhibited a size-dependent trend, with similarities emerging between carboxylated polystyrene (PS-C) 50 and 100 nm NPLs, while the smallest 30 nm NPL showed slightly distinct responses. Transcriptomic analyses reinforced these findings, revealing shared pathways across all three PS-C-NPLs —linked to cholesterol metabolism, endothelial-to-mesenchymal transition, DNA damage, and inflammation — alongside size-specific molecular signatures.

This study is the first to comprehensively link transcriptomic changes to size-dependent functional alterations in endothelial cells induced by PS-C-NPLs. Our findings demonstrate that PS-C-NPLs significantly impair endothelial cell function and integrity in a size-dependent manner, underscoring their potential cardiovascular risks.