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Nanoplastics remodel the extracellular matrix mechanical microenvironment to activate hepatic stellate cells
Summary
Polystyrene nanoplastics — especially carboxylated PS-COOH particles — were retained in collagen hydrolysate matrices mimicking the liver's space of Disse, increasing matrix viscosity and indirectly activating hepatic stellate cells through mechanical remodeling of the extracellular matrix. This is significant for microplastic health research because it identifies a novel, indirect mechanism by which nanoplastics could initiate liver fibrosis without requiring direct cytotoxicity.
Nanoplastics, an emerging class of environmental contaminants, have become a growing concern due to their widespread distribution and potential to interfere with cellular and tissue homeostasis. The liver, as a primary site of xenobiotic metabolism and clearance, is particularly vulnerable to nanoplastic exposure. Hepatic stellate cells (HSCs) play a central role in maintaining liver extracellular matrix (ECM) homeostasis and in initiating fibrogenic responses; therefore, understanding how nanoplastics affect HSC behavior is critical for elucidating early mechanisms of nanoplastic-induced liver injury. To achieve physiologically relevant modeling, we employed HSC and collagen hydrolysate to construct a simplified matrix–cell–matrix mimicking the microenvironment of the hepatic space of Disse, we found that both aminated (PS-NH2) and carboxylated (PS-COOH) polystyrene nanoplastics were retained within collagen hydrolysate matrices and altered their viscoelastic properties, with more significantly negatively charged PS-COOH increasing matrix viscosity. HSCs cultured within PS-COOH–treated matrices exhibited enhanced proliferation and migration without apparent cytotoxicity, accompanied by intensified F-actin stress fiber formation and nuclear translocation of the mechanosensitive coactivator yes-associated protein (YAP). Together, these findings indicate that nanoplastics may indirectly activate quiescent HSCs by remodeling ECM mechanical properties, rather than through direct cellular uptake. This work provides a mechanobiological perspective linking environmental nanoplastic exposure to early hepatic fibrogenesis.