We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Real-life nanoplastics induce endothelial dysfunction in primary human endothelial cells
AI summary Read the abstract
Researchers exposed primary human vascular endothelial cells to four nanoplastic types of similar size but varying environmental realism, finding that irregularly shaped PET and PTFE particles derived from real-world sources triggered IL-6 secretion, intracellular cholesterol accumulation, and impaired cell migration — functional markers of endothelial dysfunction — while more uniform pristine polystyrene did not.
Understanding how nanoplastics (NPLs) exposure affects vascular endothelium is essential for determining their potential cardiovascular risk. To this end, four different NPLs of similar nominal sizes (about 200 nm), but different environmental relevance, have been used. They are: (i) spherical and monodisperse pristine polystyrene (PS), (ii) biodegradable polylactic acid (PLA), (iii) moderately irregular and polydisperse polytetrafluoroethylene (PTFE), and (iv) highly irregular and polydisperse polyethylene terephthalate (PET) derived from post-consumer bottles. To determine their hazardous risk, primary human umbilical vein endothelial cells (HUVECs) were used as a physiologically relevant model of the vascular endothelium. Results show that all NPLs were internalized by HUVECs, although uptake efficiency and intracellular distribution varied among polymers. None of the NPLs induced cytotoxicity or DNA damage at 25 µg/mL for 24 h. However, PTFE- and PET-NPLs elicited functional alterations consistent with endothelial dysfunction. PET-NPLs triggered IL-6 secretion and intracellular cholesterol accumulation, while both PTFE- and PET-NPLs significantly impaired cell migration, reducing wound closure. These findings reveal a clear gradient of biological impact, with irregular NPLs inducing stronger endothelial stress responses. By linking morphological realism to vascular inflammation, cholesterol dysregulation, and impaired migration, this study underscores the relevance of environmentally realistic NPLs into human health risk assessment frameworks.
More Papers Like This
Transcriptomic and functional profiling of endothelial dysfunction induced by polystyrene nanoplastics
AI summary Read the abstract
Researchers exposed primary human endothelial cells to carboxylated polystyrene nanoplastics and integrated RNA sequencing with functional assays, finding coordinated dysregulation of cholesterol homeostasis, DNA repair, inflammatory signaling, and endothelial-to-mesenchymal transition — with functional readouts including intracellular cholesterol accumulation, DNA damage, and altered angiogenic behavior confirming the transcriptomic findings.
Characterization of microparticles derived from waste plastics and their bio‐interaction with human lung A549 cells
AI summary Read the abstract
Researchers characterized secondary microplastics derived from waste plastics and studied their interaction with human lung cells, finding that irregularly shaped particles from real-world plastic waste induced different biological responses than the uniform spheres typically used in laboratory studies.
Nanoplastic ShapeEffects on Lipid Bilayer Permeabilization
AI summary Read the abstract
Researchers investigated how nanoplastic shape affects lipid bilayer permeabilisation, demonstrating that morphologically diverse environmental nanoplastics interact with cell membranes in ways that differ substantially from the uniform polystyrene nanospheres typically used in laboratory studies.
Polystyrene microplastic particles induce endothelial activation
AI summary Read the abstract
Researchers found that polystyrene microplastic particles triggered inflammatory activation in endothelial cells lining blood vessels, increasing adhesion molecule expression and promoting leukocyte attachment. In mice, microplastic exposure led to elevated inflammatory cytokine and adhesion molecule expression in the aorta. The study identifies microplastics as a potential new environmental risk factor for vascular inflammation.
Nanoplastics affect the inflammatory cytokine release by primary human monocytes and dendritic cells
AI summary Read the abstract
Researchers exposed primary human immune cells to nanoplastics of different shapes, sizes, and polymer types and measured their inflammatory responses. Irregular PVC fragments triggered the strongest release of inflammatory signaling molecules, and fragment-shaped particles consistently provoked more inflammation than spherical ones. The findings indicate that the type and shape of nanoplastics matter significantly for immune responses, and that studies using only smooth spherical particles may underestimate the real-world inflammatory potential of plastic pollution.
Research digests by email
When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.