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Technical Refinement of a Bilateral Renal Ischemia-Reperfusion Mouse Model for Acute Kidney Injury Research
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Pharmacological Inhibition of PTEN Aggravates Acute Kidney Injury

Jun Zhou1,2, Li Jia1, Zhaoyong Hu1

  • 1Selzman Institute for Kidney Health and Section of Nephrology, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA.

Scientific Reports
|August 27, 2017
PubMed

Insights

PTEN inhibition worsens kidney injury following ischemia/reperfusion by increasing cell death and inflammation. This suggests PTEN is a potential therapeutic target for acute kidney injury (AKI).

Area of Science:

  • Nephrology
  • Molecular Biology
  • Pathology

Background:

  • Renal ischemia/reperfusion (I/R) is a primary cause of acute kidney injury (AKI).
  • The precise mechanisms driving renal I/R injury (IRI) remain incompletely understood.
  • PTEN, a phosphatase regulating cell signaling, has an uncharacterized role in IRI.

Purpose of the Study:

  • To investigate the role of PTEN in the pathogenesis of ischemic AKI.
  • To determine if PTEN inhibition affects renal dysfunction, tubular damage, and inflammation during IRI.

Main Methods:

  • Used a mouse model of renal IRI.
  • Administered a PTEN inhibitor (bpV(HOpic)) or vehicle.
  • Assessed renal dysfunction, tubular injury, apoptosis (caspase-3 activation), and inflammatory cell infiltration (neutrophils, macrophages) and markers.

Main Results:

  • Pharmacological PTEN inhibition exacerbated renal dysfunction and tubular damage in mice with IRI.
  • PTEN inhibition increased tubular cell apoptosis and caspase-3 activation.
  • PTEN inhibition promoted neutrophil and macrophage infiltration and elevated proinflammatory molecule expression in kidneys with IRI.

Conclusions:

  • PTEN plays a critical role in the pathogenesis of ischemic AKI.
  • PTEN regulates tubular cell apoptosis and inflammation during IRI.
  • PTEN represents a potential therapeutic target for mitigating ischemic AKI.

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