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논문분류	춘계학술대회 초록집
제목	The Role of Urine-Derived Stem Cells in Diabetes-Induced Kidney Disease(mesangial cell) Models
저자	Yoon Kyung Chang
출판정보	2026; 2026(1):
키워드	urine-derived stem cells , mesangial cell injury , hyperglycemia , diabetic nephropathy, cell cycle
초록	Objectives: Under hyperglycemic conditions, mesangial ((MES) cells promote fibrotic responses through excessive extracellular matrix (ECM) accumulation, enhanced inflammatory signaling, and activation of the TGF-β/Smad and Akt/mTOR/FOXO pathways. UDSCs are stem cells with high renal cell affinity and exhibit Klotho-mediated antifibrotic and antioxidative properties. In this study, we investigated co-culture of MES cells with UDSCs under hyperglycemic conditions might have protection as a novel therapeutic strategy for diabetic nephropathy. Methods: Urine-derived stem cells (UDSCs) were obtained through American Type Culture Collection (ATCC). Human glomerular MES cells were cultured, and high-glucose conditions were established to model the hyperglycemic environment of diabetic nephropathy. MES cells were then co-cultured with UDSCs under high-glucose conditions. Pathological and molecular changes were assessed by analyzing key fibrotic signaling pathways, including SOX9, transforming growth factor-β (TGF-β), and Smad2/3, as well as activation of the Akt/mTOR/FOXO pathway (Akt, mTOR, FOXO) and the MAPK signaling pathway (Raf, ERK). Results: MES cells exhibited characteristic spindle-shaped morphology and expressed α-SMA and fibronectin, confirming mesangial identity, while UDSCs showed a typical mesenchymal stem cell phenotype with high expression of CD73, CD90, CD105, CD146, SSEA-4, and CD24/CD133. Exposure of MES cells to high glucose established a reproducible hyperglycemia-induced injury model, characterized by structural alteration, hyperproliferation, and fibrotic changes, with 10 mM glucose identified as the optimal condition. Fig 1 UDSC co-culture under high-glucose conditions preserved MES cell morphology, suppressed abnormal proliferation and ECM accumulation, restored Akt/mTOR/FOXO protective signaling, and inhibited TGF-β/Smad and Raf/ERK fibrotic pathways Fig2 Conclusion: Notably, we demonstrate that UDSCs effectively attenuate MES cell injury by suppressing ECM accumulation, downregulating the TGF-β/Smad and Akt/mTOR pathways, and activating protective signaling mediated by FOXO and Klotho. These findings provide compelling scientific evidence supporting UDSCs as a novel and promising cell-based therapeutic candidate for DN.
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