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Polystyrene microplastic particles induce endothelial activation
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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.
Due to its increasing production, durability and multiple applications, plastic is a material we encounter every day. Small plastic particles from the μm to the mm range are classified as microplastics and produced for cosmetic and medical products, but are also a result of natural erosion and decomposition of macroplastics. Although being omnipresent in our environment and already detected in various organisms, less is known about the effects of microplastics on humans in general, or on vascular biology in particular. Here we investigated the effects of carboxylated polystyrene microplastic particles (PS, 1 μm) on murine endothelial and immune cells, which are both crucially involved in vascular inflammation, using in vitro and in vivo approaches. In vitro, PS induced adhesion molecule expression in endothelial cells with subsequent adhesion of leukocytes both under static and flow conditions. In monocytic cells, PS enhanced pro-inflammatory cytokine expression and release. Accordingly, administering mice with PS led to enhanced aortic expression of cytokines and adhesion molecules. Furthermore, we identified neutrophils as the PS-clearing blood leukocyte population. The findings from this study for the first time indicate polystyrene microplastic as a new environmental risk factor for endothelial inflammation.
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Nanoplastic-induced vascular endothelial injury and coagulation dysfunction in mice
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Researchers exposed mice to polystyrene nanoplastics with different surface modifications and found that the particles caused structural damage to vascular endothelial cells and triggered inflammatory responses. The nanoplastics also disrupted blood coagulation function in the mice. The study suggests that nanoplastic exposure may pose risks to cardiovascular health due to the particles' ability to travel through the bloodstream and damage blood vessel linings.
Polystyrene microplastic uptake drives Inflammatory, Epitranscriptomic, and Metabolic Reprogramming in Human Aortic Endothelial cells.
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Scientists found that tiny plastic particles can get inside cells lining our blood vessels, where they trigger inflammation, mess with cell metabolism, and alter how genes are processed. These changes overlap with patterns seen in real human plaques from clogged arteries, suggesting microplastics could contribute to heart disease risk, though more research is needed to confirm this in living people.
PB1065 Microvesicles Display Opposite Coagulolytic Balances According to Their Cellular Origin and Activation Status
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Polystyrene microplastics activated human vascular endothelial cells, upregulating inflammation markers ICAM-1 and VCAM-1, and promoted larger and denser blood clot formation when added to whole blood perfused over collagen at concentrations found in human plasma. These results raise concern that microplastics circulating in human blood could increase the risk of thrombosis and cardiovascular events.
Polystyrene microplastics uptake drives Inflammatory, Epitranscriptomic, and Metabolic Reprogramming in Human aortic endothelial cells
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Scientists found that tiny plastic particles (the kind found in everyday pollution) can get inside the cells lining our blood vessels and trigger inflammation, mess with cell chemistry, and even alter how genes are read—changes that overlap with what's seen in artery-clogging plaque. This was a lab study on human cells, not people directly, but it offers an early clue for how microplastics might contribute to heart disease risk, making it a reason to keep researching—and reducing—our everyday plastic exposure.
Evaluation of toxicity of polystyrene microplastics under realistic exposure levels in human vascular endothelial EA.hy926 cells
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Researchers exposed human vascular endothelial cells to polystyrene microplastics at concentrations comparable to levels detected in human blood. They found that the microplastics caused oxidative stress, reduced antioxidant defenses, and triggered apoptosis in the vascular cells. The study suggests that microplastics circulating in the bloodstream at realistic concentrations may contribute to vascular damage by impairing cellular protective mechanisms.
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