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Role of matrix metalloproteinases in viral-associated glomerulonephritis

Markus Wörnle1, Maximilian Roeder, Matthias Sauter

  • 1Medizinische Poliklinik-Klinikum der LMU, Pettenkoferstrasse 8a, 80336 München, Germany. Markus.Woernle@med.uni-muenchen.de

Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association
|November 14, 2008
PubMed
Abstract

Insights

Viral RNA activates specific receptors on mesangial cells, increasing MMP9 expression and contributing to glomerular fibrosis. This suggests a new link between viral infections and kidney disease progression.

Area of Science:

  • Nephrology
  • Virology
  • Molecular Biology

Background:

  • Viral infections frequently cause virus-associated glomerulonephritis, a condition marked by renal failure due to glomerular and interstitial fibrosis.
  • Fibrosis in advanced glomerular disease involves extracellular matrix accumulation, regulated by matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinase (TIMPs).

Purpose of the Study:

  • To investigate the role of viral receptors in modulating matrix metalloproteinase (MMP) and tissue inhibitor of metalloproteinase (TIMP) expression in human mesangial cells.
  • To explore the link between viral infections and the pathogenesis of glomerular fibrosis.

Main Methods:

  • Reverse transcription-polymerase chain reaction (RT-PCR) was used to analyze the expression of MMP2, MMP9, and TIMP-1 in cultured human mesangial cells.
  • Knockdown experiments utilizing small interfering RNA (siRNA) targeting toll-like receptor 3 (TLR3) and RIG-I were performed to elucidate the specific roles of these viral receptors.

Main Results:

  • Human mesangial cells express viral receptors toll-like receptor 3 (TLR3) and RIG-I.
  • Activation of TLR3 and RIG-I by viral RNA (poly (I:C) RNA) induced a time- and dose-dependent increase in MMP9 expression.
  • MMP2 and TIMP-1 expression remained unaffected, and knockdown of TLR3 and RIG-I confirmed their specific roles in MMP9 induction.

Conclusions:

  • Glomerular mesangial cells possess functional viral sensors (TLR3 and RIG-I) that can be activated by viral RNA.
  • This activation leads to increased MMP9 expression, suggesting a novel mechanism linking viral infections to glomerular inflammation and fibrosis.
  • These findings highlight a potential pathophysiologic role for viral receptors in the development of virus-associated glomerulonephritis.

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