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MMP9 and SCF protect from apoptosis in acute kidney injury

Soraya Bengatta1, Catherine Arnould, Emmanuel Letavernier

  • 1UPMC University of Paris 06, Paris, France.

Journal of the American Society of Nephrology : JASN
|March 31, 2009
PubMed

Insights

Matrix metalloproteinase 9 (MMP9) protects kidney cells from apoptosis in acute kidney injury (AKI) by releasing soluble stem cell factor (sSCF). MMP9 deficiency worsens AKI, while sSCF shows therapeutic potential.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Cellular Biology

Background:

  • Apoptosis of tubular epithelial cells is a key feature of acute kidney injury (AKI).
  • The precise cellular mechanisms preceding apoptosis in AKI remain unclear.
  • Matrix metalloproteinase 9 (MMP9) plays a role in degrading matrix components crucial for cell survival.

Purpose of the Study:

  • To investigate the role of MMP9 in the pathogenesis of AKI.
  • To determine the protective mechanisms of MMP9 in kidney injury.
  • To explore the potential of stem cell factor (SCF) as a therapeutic target in AKI.

Main Methods:

  • Utilized a mouse model of folic acid-induced AKI and an ischemia-reperfusion model.
  • Assessed MMP9 activity, apoptosis markers, and renal function in wild-type and MMP9-deficient mice.
  • Investigated the interaction between MMP9, SCF, and its receptor c-Kit in kidney cells.
  • Measured urinary soluble SCF (sSCF) levels in AKI patients.

Main Results:

  • MMP9 activity increased in the S3 segment of proximal tubules during AKI.
  • MMP9 deficiency exacerbated apoptosis, renal lesions, and delayed functional recovery.
  • MMP9 released SCF, which inhibited tubular cell apoptosis and improved renal function.
  • Urinary sSCF levels were elevated in patients with acute tubular necrosis.

Conclusions:

  • MMP9 is protective against apoptosis in the S3 segment of proximal tubules and collecting duct intercalated cells during AKI.
  • The protective effect of MMP9 is mediated, at least in part, by the release of soluble SCF.
  • SCF holds potential as a biomarker and therapeutic agent for AKI.

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