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Acute Kidney Injury Model Induced by Cisplatin in Adult Zebrafish
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PLK2 targets GSK3β to protect against cisplatin-induced acute kidney injury

Xiaona Wei1, Jianping Wu1, Jiajia Li1

  • 1Department of Nephrology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.

Experimental Cell Research
|May 6, 2022
PubMed

Insights

Polo-like kinase 2 (PLK2) protects against cisplatin-induced acute kidney injury (AKI) by reducing apoptosis and oxidative stress. Upregulated PLK2 may serve as a novel therapeutic target for preventing cisplatin nephrotoxicity.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Biochemistry

Background:

  • Cisplatin-induced acute kidney injury (AKI) is a severe condition lacking effective treatments.
  • Polo-like kinase 2 (PLK2) is implicated in various disease processes.
  • Identifying novel therapeutic targets for AKI is crucial.

Purpose of the Study:

  • To investigate the role of PLK2 in cisplatin-induced AKI.
  • To determine if PLK2 could be a potential therapeutic target for cisplatin nephrotoxicity.

Main Methods:

  • Integrated two Gene Expression Omnibus (GEO) datasets for cisplatin-induced AKI models.
  • Verified PLK2 expression in AKI animal and cell models.
  • Utilized siRNAs and inhibitors to suppress PLK2; enforced PLK2 expression.
  • Investigated PLK2's potential phosphorylation of glycogen synthase kinase 3β (GSK3β).

Main Results:

  • PLK2 was significantly upregulated in AKI renal tissues.
  • PLK2 suppression exacerbated cisplatin-induced AKI, increasing apoptosis and oxidative stress.
  • Enforced PLK2 expression protected against cisplatin-induced renal dysfunction.
  • PLK2 potentially phosphorylates GSK3β in AKI pathogenesis.

Conclusions:

  • PLK2 plays a protective role in cisplatin-induced AKI.
  • PLK2 represents a potential therapeutic target for mitigating cisplatin nephrotoxicity.
Keywords:
Acute kidney injuryApoptosisCisplatinGlycogen synthase kinase 3βOxidative stressPolo-like kinase 2

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