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Single-cell RNA-seq analysis decodes the kidney microenvironment induced by polystyrene microplastics in mice receiving a high-fat diet
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Using advanced single-cell gene analysis, researchers found that mice fed both polystyrene microplastics and a high-fat diet suffered significantly worse kidney damage than either exposure alone. The combination reshaped the kidney's cellular environment, promoting scarring, triggering cancer-related pathways, and altering immune cell populations. This is particularly relevant to human health because many people are simultaneously exposed to microplastics through food and drink while also consuming high-fat diets.
In recent years, the environmental health issue of microplastics has aroused an increasingly significant concern. Some studies suggested that exposure to polystyrene microplastics (PS-MPs) may lead to renal inflammation and oxidative stress in animals. However, little is known about the essential effects of PS-MPs with high-fat diet (HFD) on renal development and microenvironment. In this study, we provided the single-cell transcriptomic landscape of the kidney microenvironment induced by PS-MPs and HFD in mouse models by unbiased single-cell RNA sequencing (scRNA-seq). The kidney injury cell atlases in mice were evaluated after continued PS-MPs exposure, or HFD treated for 35 days. Results showed that PS-MPs plus HFD treatment aggravated the kidney injury and profibrotic microenvironment, reshaping mouse kidney cellular components. First, we found that PS-MPs plus HFD treatment acted on extracellular matrix organization of renal epithelial cells, specifically the proximal and distal convoluted tubule cells, to inhibit renal development and induce ROS-driven carcinogenesis. Second, PS-MPs plus HFD treatment induced activated PI3K-Akt, MAPK, and IL-17 signaling pathways in endothelial cells. Besides, PS-MPs plus HFD treatment markedly increased the proportions of CD8 effector T cells and proliferating T cells. Notably, mononuclear phagocytes exhibited substantial remodeling and enriched in oxidative phosphorylation and chemical carcinogenesis pathways after PS-MPs plus HFD treatment, typified by alterations tissue-resident M2-like PF4 macrophages. Multispectral immunofluorescence and immunohistochemistry identified PF4 macrophages in clear cell renal cell carcinoma (ccRCC) and adjacent normal tissues, indicating that activate PF4 macrophages might regulate the profibrotic and pro-tumorigenic microenvironment after renal injury. In conclusion, this study first systematically revealed molecular variation of renal cells and immune cells in mice kidney microenvironment induced by PS-MPs and HFD with the scRNA-seq approach, which provided a molecular basis for decoding the effects of PS-MPs on genitourinary injury and understanding their potential profibrotic and carcinogenesis in mammals.
More Papers Like This
Additional file 1 of Single-cell RNA-seq analysis decodes the kidney microenvironment induced by polystyrene microplastics in mice receiving a high-fat diet
AI summary Read the abstract
Researchers used single-cell RNA sequencing to decode kidney microenvironmental changes induced by polystyrene microplastics in mice fed a high-fat diet, characterizing mural cell and mesangial cell heterogeneity, DEG profiles, and pathway enrichment in affected renal tissue.
Exploring the Mechanism of Kidney Injury in Mice Induced by High-Fat Diet and Polystyrene Nanoplastics Co-Exposure Through the Kidney-Gut Axis
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In a mouse study, the combination of a high-fat diet and polystyrene nanoplastics caused worse kidney damage than either exposure alone, working through the kidney-gut connection. The nanoplastics plus high-fat diet disrupted gut bacteria, increased inflammation, and triggered a harmful immune response that traveled from the gut to the kidneys. This suggests that people who eat high-fat diets may be more vulnerable to kidney damage from nanoplastic exposure.
Exploring the Mechanismof Kidney Injury in Mice Inducedby High-Fat Diet and Polystyrene Nanoplastics Co-Exposure Throughthe Kidney-Gut Axis
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This mouse study found that combining a high-fat diet with polystyrene nanoplastic exposure (100 nm, 25 mg/kg/day) worsened kidney toxicity beyond high-fat diet alone, with the combination disrupting lipid metabolism via tryptophan and glycerophospholipid pathways and exacerbating gut microbiota dysbiosis through the kidney-gut axis.
Effects of Microplastic (MP) Exposure at Environmentally Relevant Doses on the Structure, Function, and Transcriptome of the Kidney in Mice
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Researchers exposed mice to polystyrene microplastics at doses matching levels found in the environment and examined the effects on kidney structure and function. While the microplastics did not cause obvious physical damage to the kidneys, they altered blood markers of kidney function and changed gene expression patterns related to immune response and metabolism. The study suggests that even low-level microplastic exposure may subtly affect kidney biology at the molecular level.
Single-cell transcriptome analysis of liver immune microenvironment changes induced by microplastics in mice with non-alcoholic fatty liver
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Using advanced single-cell analysis, researchers showed that microplastics worsened non-alcoholic fatty liver disease in mice fed a high-fat diet by changing how immune cells behaved in the liver. Microplastic exposure amplified inflammatory responses and altered the communication between different liver cell types. This study is important because it reveals specific immune mechanisms by which microplastics could worsen liver disease, a condition already affecting roughly one in four adults worldwide.
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