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Kidney Week

Abstract: PO0208

Protein Phosphatase 2A Cα Reprograms Cellular Energy Metabolism to Promote Tubular Cell Death and Kidney Injury

Session Information

  • AKI Mechanisms - 2
    October 22, 2020 | Location: On-Demand
    Abstract Time: 10:00 AM - 12:00 PM

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms

Authors

  • Gu, Mengru, Nanjing Medical University, Nanjing, Jiangsu, China
  • Dai, Chunsun, Nanjing Medical University, Nanjing, Jiangsu, China
Background

Protein phosphatase 2A (PP2A), one of the primary serine-threonine phosphatases in mammalian cells, regulates various biological processes. The role and mechanisms for PP2A in kidney injury remains to be determined.

Methods

Generating the mice with PP2Aca ablation with Cre-Loxp system. Mice were injected with cisplatin to induce AKI. UUO was performed on the mice to induce kidney fibrosis.

Results

In this study, we found that the expression of protein phosphatase 2A Cα (PP2Acα) in tubular cells was upregulated in both patients and animal models with acute and chronic kidney injury. Ablation of PP2Aca in tubular cells alleviated cisplatin-induced acute kidney injury and unilateral ureteral obstruction-induced kidney fibrosis in mice. In cultured tubular cells, ablation of PP2Acα promotes oxidative phosphorylation of fatty acids by increasing p-ACC levels and thus protects against cisplatin-induced cell death and TGFβ1-induced fibronectin production.

Conclusion

This study reveals the essential role for PP2Acα in regulating tubular cell energy metabolism and survival, which may shed light on treating patients with kidney injury.