Abstract: SA-PO076
Neutrophil Extracellular Traps Promote Polyploidization of Tubular Epithelial Cells after Kidney Injury
Session Information
- AKI: Inflammation and Cell Cycle
October 26, 2024 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 103 AKI: Mechanisms
Authors
- Li, Wenchao, Sun Yat-Sen Memorial Hospital, Guangzhou, Guangdong, China
- Hao, Li, Sun Yat-Sen Memorial Hospital, Guangzhou, Guangdong, China
- Gan, Yangang, Sun Yat-Sen Memorial Hospital, Guangzhou, Guangdong, China
- Li, Jiajia, Sun Yat-Sen Memorial Hospital, Guangzhou, Guangdong, China
- Yu, Hao, Sun Yat-Sen Memorial Hospital, Guangzhou, Guangdong, China
- Han, Qianqian, Sun Yat-Sen Memorial Hospital, Guangzhou, Guangdong, China
- Zeng, Weicong, Sun Yat-Sen Memorial Hospital, Guangzhou, Guangdong, China
- Yang, Qiongqiong, Sun Yat-Sen Memorial Hospital, Guangzhou, Guangdong, China
Background
Renal tubular epithelial cells undergo polyploidization after acute kidney injury (AKI), which promotes tubular cell senescence and renal fibrosis, the underlying mechanism remains unclear. Neutrophil extracellular traps (NETs) play a crucial role in tubular injury after AKI, but whether NETs promote tubular cell polyploidization is uncear.
Methods
The expression of NETs and polyploid tubules were analysed in renal ischemia-reperfusion (IRI) model. DNase I was emplayed as inhibitor of NETs, and the effects of tubular cell polyploidization and renal fibrosis was detected.
Results
The expression of NETS and polyploid tubular cells were upregulated after AKI. Clearing NETs decreased the amount of polyploid tubules and ameliorated renal fibrosis.
Conclusion
NETs regulate the transition from AKI to CKD by promoting polyploidization of renal tubular cells.
Expression of NETs and polyploid tubular cells in IRI model
Removal of NETs decreased polyploid tubular cell formation in IRI model