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논문분류	춘계학술대회 초록집
제목	Particulate Matter Induces Epithelial-to-Mesenchymal Transition by Oxidative and Endoplasmic Reticulum Stress in Normal Rat Kidney Epithelial Cells
저자	Chor Ho Jo
출판정보	2025; 2025(1):
키워드	Artificial particulate matter, Epithelial-to-mesenchymal transition, Oxidative stress, Endoplasmic reticulum stress, Normal rat kidney epithelial cells
초록	Particulate matter (PM) exposure has been linked to respiratory, cardiovascular, and kidney diseases. However, its direct role in kidney disease remains unclear. Oxidative stress, endoplasmic reticulum (ER) stress, and epithelial-to-mesenchymal transition (EMT) are key mechanisms for renal injury. This study investigated the effects of artificially manufactured PM (APM) on renal tubular epithelial cells. APM (provided by the Korea Institute of Toxicology) was dissolved in DMSO via sonication. Normal rat kidney epithelial (NRK) cells were treated with APM at 1, 2, and 5 μg/mL. Cytotoxicity and proliferation were assessed using LDH release and MTS assay. EMT was evaluated by morphological changes and expression of EMT markers (E-cadherin, α-SMA, and fibronectin) using western blotting, qPCR, and immunostaining. Reactive oxygen species (ROS) generation was measured using DCF-DA and MitoSOX staining. Antioxidants [N-acetylcysteine (NAC), 20 mM; apocynin, 100 uM] and ER stress inhibitors [tauroursodeoxycholic acid (TUDCA), 1 mM, 4-phenylbutyric acid (4-PBA), 5 mM] were used to examine their effects on EMT, NOX1/4 expression, and NLRP3 inflammasome activation in APM-exposed NRK cells at 24 or 48 hours. APM (1, 2, and 5 μg/mL) exposure for up to 24 hours did not alter LDH release or cell proliferation. APM induced EMT of NRK cells from 2 μg/mL shown as morphological alterations, decreased E-cadherin expression, and de novo expressions of α-SMA and fibronectin. Treatment with antioxidants (NAC and apocynin) and ER stress inhibitors (TUDCA and 4-PBA) mitigated APM-induced EMT, which was accompanied with reductions in NOX1/4 expression and NLRP3 inflammasome activation (NLRP3, ASC, and cleaved caspase-1) at 24 and 48 hours. These findings suggest that APM induces EMT via oxidative and ER stress in NRK cells, highlighting a potential mechanism for air pollution-induced kidney disease.
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