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논문분류	춘계학술대회 초록집
제목	PM2.5 Induced Phenotype Transition of Renal Tubular Epithelial Cells Via Oxidative Stress
저자	Dal-Ah Kim
출판정보	2025; 2025(1):
키워드	Particulate matter, Oxidative stress, Epithelial-to-mesenchymal transition, RNA-seq
초록	The incidence and prevalence of chronic kidney disease (CKD) are rising worldwide. Recently, exposure to fine particulate matter, particularly PM2.5, has been identified as a risk factor for CKD development and progression. However, it remains unclear whether PM2.5 exposure directly contributes to kidney disease. Epithelial-to-mesenchymal transition (EMT) of renal tubular cells is recognized as an early mechanism of renal injury. This study aims to investigate whether PM2.5 induces EMT in renal tubular epithelial cells through oxidative stress. PM2.5 samples collected from Ulaanbaatar, Mongolia, were dissolved in DMSO using sonication. Normal rat kidney (NRK) tubular epithelial cells were treated with PM2.5 (2 & 5 μL/mL). EMT was evaluated by assessing morphological changes and analyzing the expression levels of E-cadherin, α-SMA, and vimentin via western blotting and immunostaining. Reactive oxygen species (ROS) generation was measured using DCF-DA and MitoSox staining. Additionally, RNA-seq was performed to identify differentially expressed genes in PM2.5-exposed NRK cells. PM2.5 (2 and 5 μL/mL) did not affect LDH release or cell proliferation for up to 48 hours. However, PM2.5 induced EMT in NRK cells, as evidenced by morphological changes, decreased E-cadherin expression, and de novo expression of α-SMA and vimentin. PM2.5 also led to increased ROS production, as indicated by enhanced DCF-DA and Mito-Sox staining. RNA-seq analysis revealed significant alterations in gene expression related to EMT (16.7%), adipokine (15.9%), apoptosis (13.7%), and oxidative stress (12.8%). Among the differentially expressed genes, Lipocalin-2, Interleukin-11, and hyaluronan synthase-2 exhibited the highest fold changes (2.7-folds, 2.5-folds, and 2.0-folds, respectively) in PM2.5-exposed NRK cells compared to control cells. These findings suggest that PM2.5 induces EMT and oxidative stress in renal tubular epithelial cells, highlighting a potential causal link between fine dust and kidney disease. Furthermore, phenotype transition and oxidative stress may serve as therapeutic targets for PM2.5-induced kidney disease.
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