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논문분류	춘계학술대회 초록집
제목	Dapagliflozin Attenuates PM2.5-Induced Renal Tubular Cell Injury via Modulation of EGR-1 and MAPK Signaling Pathways
저자	Hyung Eun Yim
출판정보	2026; 2026(1):
키워드	Airborne Particulate Matter, Early Growth Response Protein 1, Extracellular Signal Regulated MAP Kinases, Kidney, Sodium-Glucose Transporter 2
초록	Objectives: Dapagliflozin (DAPA), a sodium–glucose co-transporter 2 inhibitor, demonstrates renoprotective properties across various kidney diseases. Early growth response-1 (EGR-1), a transcription factor, exerts context-dependent roles in regulating inflammatory responses and tissue repair. This study examined fine particulate matter (PM₂.₅)-induced mitogen-activated protein kinase (MAPK) activation and inflammation in human renal proximal tubular cells, focusing on EGR-1 regulation and the potential protective effects of DAPA. Methods: HK-2 cells were exposed to PM₂.₅ with or without DAPA (40 μM) for 48 h. Cytotoxicity was measured using a cell counting kit-8 assay. EGR-1 and extracellular signal-regulated kinase (ERK) activities were assessed over PM₂.₅ exposure time. Western blotting was performed for EGR-1, ERK, p38, c-Jun N-terminal kinase, intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1. MAPK activity was further examined following EGR-1 knockdown or overexpression, with or without PM₂.₅. Results: PM₂.₅ reduced the viability of HK-2 cells in a dose- and time-dependent manner. EGR-1 exhibited an initial transient increase followed by a decline, whereas the phosphorylated ERK (p-ERK)/total ERK (t-ERK) ratio progressively increased. After 48 h, p-ERK/t-ERK, phosphorylated p38 (p-p38)/total p38 (t-p38), and ICAM-1 levels were elevated, while EGR-1 activity was reduced. EGR-1 silencing enhanced the p-ERK/t-ERK ratio, and PM₂.₅ further increased this ratio irrespective of EGR-1 status. DAPA improved cell viability, restored EGR-1 activity, and reduced p-ERK/t-ERK and p-p38/t-p38 ratios. Conclusion: PM₂.₅ induces a rapid, transient EGR-1 activation, followed by sustained MAPK signaling and inflammatory adhesion molecule expression. DAPA alleviates PM₂.₅-induced cytotoxicity by suppressing ERK and p38 activation and restoring EGR-1, indicating its therapeutic potential against PM₂.₅-mediated renal tubular cell injury.
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