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Deletion of p18(INK4c) aggravates cisplatin-induced acute kidney injury

Liang Wang1, Wei Chen2, Yi Zhang2

  • 1Department of Urology, The Second Affiliated Hospital of Dalian Medical University, Dalian 116021, P.R. China.

International Journal of Molecular Medicine
|April 10, 2014
PubMed

Insights

The INK4 family member p18 (INK4c) protects against acute kidney injury (AKI). Deleting p18 worsened kidney damage and survival in cisplatin-induced AKI, suggesting p18

Area of Science:

  • Nephrology
  • Molecular Biology
  • Cellular Stress Response

Background:

  • Cyclin-dependent kinase inhibitors (CDKIs) show protective effects in acute kidney injury (AKI).
  • Research on CDKIs in AKI has primarily focused on CIP/KIP family members.
  • The role of INK4 family members, specifically p18(INK4c) (p18), in AKI remains under-investigated.

Purpose of the Study:

  • To investigate the role of p18(INK4c) in cisplatin-induced acute kidney injury (AKI).
  • To evaluate the protective effects of p18 in a mouse model of AKI.
  • To explore the association between p18 expression and endoplasmic reticulum stress (ERS) in AKI.

Main Methods:

  • Utilized p18 gene knockout mice (p18-/-) and wild-type (p18+/+) littermates.
  • Induced AKI via a single intraperitoneal injection of cisplatin (12.5 mg/kg).
  • Assessed survival rates, renal function (e.g., serum creatinine, BUN), morphological kidney injuries, and endoplasmic reticulum stress markers (Western blot).

Main Results:

  • Mice lacking p18 (p18-/-) exhibited significantly reduced survival rates compared to wild-type mice (p18+/+) following cisplatin administration.
  • p18 deletion exacerbated renal function impairment and morphological damage in cisplatin-induced AKI.
  • The absence of p18 significantly aggravated endoplasmic reticulum stress (ERS) in the kidneys of AKI mice.

Conclusions:

  • p18(INK4c) exerts a protective role in cisplatin-induced acute kidney injury.
  • The protective mechanism of p18 may involve the regulation of cell death pathways, particularly endoplasmic reticulum stress.
  • These findings highlight p18 as a potential therapeutic target for AKI.

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