Neutrophil Extracellular Traps Promote Polyploidization of Tubular Epithelial Cells after Kidney Injury

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 modelRemoval of NETs decreased polyploid tubular cell formation in IRI model

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Journal
Journal of the American Society of Nephrology
Published
2024-10-01
DOI
https://doi.org/10.1681/asn.202411ejq3eh
Primary Topic
Neutrophil, Myeloperoxidase and Oxidative Mechanisms
Type
article
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article

Neutrophil Extracellular Traps Promote Polyploidization of Tubular Epithelial Cells after Kidney Injury

Yangang Gan, Qianqian Han, Wenchao Li, Hao Yu et al.
Journal of the American Society of Nephrology
Neutrophil, Myeloperoxidase and Oxidative Mechanisms
article

Neutrophil Extracellular Traps Promote Polyploidization of Tubular Epithelial Cells after Kidney Injury

Yangang Gan, Qianqian Han, Wenchao Li, Hao Yu, Hao Li, Wen Zeng, Qiongqiong Yang, Jiajia Li
article en

Abstract

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 modelRemoval of NETs decreased polyploid tubular cell formation in IRI model

Journal of the American Society of NephrologyVol. 35(10S)
Sun Yat-sen University (CN), Sun Yat-sen Memorial Hospital (CN)
Good health and well-being
Openalex Percentile: Top 76%
Neutrophil, Myeloperoxidase and Oxidative Mechanisms
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