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Polystyrene microplastic-induced extracellular vesicles cause kidney-related effects in the crosstalk between tubular cells and fibroblasts

Ecotoxicology and Environmental Safety 2024 25 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 65 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Hui‐Wen Chiu, Yung‐Li Wang, Yung‐Li Wang, Wen‐Chih Liu, Yung‐Li Wang, Yung‐Li Wang, Yu‐Hsuan Lee, Yu‐Hsuan Lee, Cai‐Mei Zheng, Yu‐Hsuan Lee, Cathy Chia‐Yu Huang Wen‐Chih Liu, Cai‐Mei Zheng, Yung‐Li Wang, Yung‐Li Wang, Yung‐Li Wang, Yu‐Hsuan Lee, Yu‐Hsuan Lee, Wen‐Chih Liu, Yung‐Li Wang, Hui‐Wen Chiu, Yu‐Hsuan Lee, Yung‐Li Wang, Hui‐Wen Chiu, Hui‐Wen Chiu, Cathy Chia‐Yu Huang Yu‐Hsuan Lee, Hui‐Wen Chiu, Yung‐Li Wang, Hui‐Wen Chiu, Yu‐Hsuan Lee, Hui‐Wen Chiu, Hui‐Wen Chiu, Cathy Chia‐Yu Huang Hui‐Wen Chiu, Cathy Chia‐Yu Huang Cathy Chia‐Yu Huang

Summary

Researchers found that polystyrene microplastics cause kidney tubule cells to release tiny signaling packages (extracellular vesicles) that trigger stress responses and scarring in neighboring kidney cells. This cell-to-cell communication pathway spread the damage beyond the cells directly exposed to the microplastics. The findings suggest a mechanism by which microplastic exposure could contribute to kidney fibrosis and long-term kidney damage in humans.

Polymers
Body Systems
Study Type In vivo

Plastic waste accumulation and its degradation into microplastics (MPs) and nanoplastics (NPs) pose environmental concerns. Previous studies have indicated that polystyrene (PS)-MPs harm living animals. Extracellular vesicles (EVs) are associated with metabolic reprogramming and mitochondrial dysfunction in various kidney diseases. In this article, we evaluated how PS-MPs affected tubular cells and fibroblasts. The results demonstrated that PS-MPs increased EV production in human tubular cells and caused endoplasmic reticulum (ER) stress-related proteins without inducing inflammation-related proteins in human tubular cells. The uptake of PS-MPs and incubation with the conditioned medium of PS-MPs induced reactive oxygen species (ROS) production and ER stress-related proteins in fibroblast cells. The fibroblast cells treated with the conditioned medium of PS-MPs also increased the expression of fibrosis-related proteins. Our findings suggested that the expression of EV-related markers increased in tubular cells via Beclin 1 after PS-MP treatment. In addition, PS-MPs induced ROS production in vitro and in vivo. We found that PS-MPs also altered the expression of EV markers in urine, and CD63 expression was also increased in vitro and in vivo after PS-MP treatment. In conclusion, PS-MP-induced EVs lead to ER stress-related proteins, ROS production and fibrosis-related proteins in tubular cells and fibroblasts.

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