ArticleKidney diseases (Basel, Switzerland)
Inhibition of Plk1 Attenuates Downregulation of Water and Sodium Transporters in Obstructive Nephropathy.
Article in Kidney diseases (Basel, Switzerland). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Obstructive nephropathy is frequently associated with downregulation of key renal water and sodium transporters, resulting in impaired urinary concentration and disrupted fluid balance. The present study aimed to investigate the role of Polo-like kinase 1 (Plk1), a kinase traditionally recognized for its function in cell-cycle regulation, in modulating renal water and sodium transporters in a unilateral ureteral obstruction (UUO) model, and to elucidate the underlying molecular mechanisms. Methods: Plk1 function was inhibited pharmacologically using BI6727 or genetically using heterozygous Plk1 knockout mice. In vitro, renal collecting duct M1 cells were stimulated with TGF-β to examine mechanistic pathways. Results: Inhibition of Plk1 with BI6727 preserved the expression of aquaporin 2 (AQP2) and sodium-potassium-chloride cotransporter 2 (NKCC2) in UUO kidneys. Similarly, heterozygous Plk1 knockout mice exhibited higher AQP2 and NKCC2 levels than wild-type controls. Mechanistically, Plk1 regulated cytosolic phospholipase A Conclusion: These findings indicate that Plk1 contributes to the maladaptive downregulation of renal water and sodium transporters during obstruction. Pharmacological inhibition or genetic reduction of Plk1 preserves transporter expression, highlighting the Plk1-cPLA
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