Abstract: SA-PO0256
Polo-Like Kinase 1 Is Upregulated in Experimental AKI and Regulates Tubular Epithelial Injury Responses
Session Information
- AKI: Mechanisms - Cell Signaling
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 103 AKI: Mechanisms
Authors
- Park, Beamjun, Soonchunhyang University Hospital Cheonan, Cheonan-si, Chungcheongnam-do, Korea (the Republic of)
- Kim, Dong Seop, Soonchunhyang University Hospital Cheonan, Cheonan-si, Chungcheongnam-do, Korea (the Republic of)
- Cho, Nam-Jun, Soonchunhyang University Hospital Cheonan, Cheonan-si, Chungcheongnam-do, Korea (the Republic of)
- Park, Samel, Soonchunhyang University Hospital Cheonan, Cheonan-si, Chungcheongnam-do, Korea (the Republic of)
- Gil, Hyo-Wook, Soonchunhyang University Hospital Cheonan, Cheonan-si, Chungcheongnam-do, Korea (the Republic of)
Background
Acute kidney injury (AKI) is driven by tubular epithelial injury and incomplete repair, but cell-cycle regulators that connect injury responses to maladaptive repair remain incompletely defined. Polo-like kinase 1 (PLK1) is a mitotic kinase involved in cell-cycle progression and stress responses. We hypothesized that PLK1 is induced in AKI and contributes to tubular injury responses across ischemic, nephrotoxic, and hypoxic injury models.
Methods
Male C57BL/6 mice underwent bilateral renal ischemia-reperfusion injury (IRI; 23-min pedicle clamping) or cisplatin-induced AKI. Kidney injury was assessed by serum creatinine, BUN, PAS-based tubular injury scoring, and KIM-1/NGAL expression. PLK1 expression was examined by qPCR, ELISA, immunohistochemistry, and immunofluorescence with proximal tubular markers. TCMK-1 tubular epithelial cells were exposed to hypoxia-reoxygenation (H/R), and H/R-induced injury, hypoxia, cell-cycle, and senescence-related responses were compared between PLK1-suppressed and control cells.
Results
Both IRI and cisplatin AKI models showed significant renal dysfunction, tubular injury, and increased KIM-1/NGAL expression compared with controls. PLK1 expression was consistently increased at the mRNA and protein levels in injured kidneys, with predominant localization to damaged proximal tubules. In public kidney organoid and human AKI transcriptomic datasets, PLK1 was enriched in cell-cycle-associated epithelial populations, supporting its injury-linked expression pattern. In TCMK-1 cells, H/R induced PLK1 together with hypoxia and injury markers. Preliminary PLK1 suppression attenuated H/R-associated injury marker expression and altered cell-cycle/senescence-related signals, suggesting a functional role for PLK1 beyond passive injury response.
Conclusion
PLK1 is reproducibly upregulated in ischemic, nephrotoxic, and hypoxic models of AKI and localizes to injured proximal tubular epithelium. These findings identify PLK1 as a candidate mediator linking tubular injury, cell-cycle dysregulation, and maladaptive repair. Further studies will define the downstream PLK1-dependent pathway that determines adaptive versus maladaptive tubular recovery after AKI.
Acknowledgment
This research was supported by Individual Basic Research Program (Mid-Career Research – Creative Research Type), the National Research Foundation of Korea(NRF) funded by the Ministry of Education(RS-20250988).
Funding
- Government Support – Non-U.S.