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The regulation of circRNA_kif26b on alveolar epithelial cell senescence via miR-346-3p is involved in microplastics-induced lung injuries
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Researchers found that inhaled polystyrene microplastics caused lung damage in rats by accelerating the aging of cells lining the air sacs, through a specific molecular pathway involving circular RNA. The microplastics triggered inflammation, fibrosis, and premature cell aging in lung tissue over a 35-day exposure period. The study reveals a new mechanism by which inhaled microplastics may contribute to lung injury.
Microplastics (MPs), the emerging environmental contaminants, can be inhaled and lead to lung injuries, including inflammation and fibrosis. Alveolar epithelial cell senescence is associated with several lung diseases, but its mechanism in MPs-induced lung injuries remains unknown. In this study, polystyrene microplastics (PS-MPs) in the form of microspheres with a particle size of 100 nm were used for a 35-day inhalation exposure in SPF-grade Sprague-Dawley (SD) rats. The plethysmograph showed lung dysfunction. The hematoxylin and eosin (H&E) staining revealed lung histological lesions with a significant accumulation of inflammatory cells. The β-galactosidase staining indicated increased senescent cells in lung tissues. The ELISA suggested increased senescence-associated secretory phenotype (SASP) in bronchoalveolar lavage fluid (BALF). Treatment of mouse alveolar epithelial cell line MLE12 with PS-MPs raised levels of senescence-related markers p21, p16, and p27 and SASP secretion. circ_kif26b, a ring-structured non-coding RNA (ncRNA), is homologous in human, rat, and mouse and was elevated in PS-MPs-exposed rat lung tissues as well as in PS-MPs-treated MLE12 cells. The luciferase reporter gene revealed that circ_kif26b was bound to miR-346-3p and co-regulated p21, a target gene of miR-346-3p. circ_kif26b knockdown or miR-346-3p overexpression attenuated PS-MPs-induced MLE12 cell senescence and secretion of the SASP cytokines IL-6 and IL-8. However, down-regulation of circ_kif26b and miR-346-3p reversed this depressive effect. Overall, circ_kif26b mediates alveolar epithelial cell senescence through miR-346-3p and participates in PS-MPs-induced lung inflammation. These findings provide new insights into the mechanisms of MPs inhalation toxicity and lay a mechanistic foundation for health risk assessment of MPs.
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Mechanism of circRNA_SMG6 mediating lung macrophage ECM degradation via miR-570-3p in microplastics-induced emphysema
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In a rat study, inhaling polystyrene microplastics for 90 days caused lung damage resembling emphysema, including inflammation, thickened tissue walls, and enlarged air sacs. The microplastics triggered the breakdown of the structural support network in the lungs through a specific molecular pathway involving circular RNA. This research provides a mechanism by which breathing in microplastic particles could contribute to chronic lung disease in humans.
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Researchers exposed rats to polystyrene microplastics through the airways and found evidence of lung tissue damage, including destroyed air sacs and inflammation. The study identified changes in the activity of long non-coding RNAs and circular RNAs, types of genetic regulators that may help explain how microplastics cause lung injury at the molecular level. These findings provide new insight into the biological mechanisms behind potential respiratory harm from inhaling microplastic particles.
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