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Advanced glycation end products decrease mesangial cell MMP-7: a role in matrix accumulation in diabetic nephropathy?

S V McLennan1, D J Kelly, M Schache

  • 1Department of Endocrinology, Royal Prince Alfred Hospital, Sydney, New South Wales, Australia. sue@med.usyd.edu.au

Kidney International
|June 8, 2007
PubMed
Summary
This summary is machine-generated.

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Diabetic kidney disease involves excess fibronectin. This study found that reduced matrix metalloproteinase-7 (MMP-7) expression, influenced by advanced glycation end products (AGEs), contributes to fibronectin accumulation in diabetic nephropathy.

Area of Science:

  • Nephrology
  • Biochemistry
  • Molecular Biology

Background:

  • Diabetic nephropathy is characterized by increased extracellular matrix, including fibronectin.
  • Degradative pathways for non-collagenous proteins in diabetes are not well understood.

Purpose of the Study:

  • To investigate the expression of matrix metalloproteinase-7 (MMP-7), a key enzyme for fibronectin degradation.
  • To explore the impact of advanced glycation end products (AGEs) on MMP expression in mesangial cells.

Main Methods:

  • Cultured human mesangial cells were exposed to AGEs.
  • MMP expression was analyzed in vitro and in streptozotocin-induced diabetic rats.
  • MMP-7 levels were assessed in human diabetic kidney samples.

Related Experiment Videos

Main Results:

  • AGEs significantly reduced MMP-7 expression in mesangial cells.
  • Aminoguanidine and anti-transforming growth factor-beta (TGF-beta) antibody normalized MMP-7 levels.
  • Reduced MMP-7 and increased fibronectin were observed in diabetic rats and humans with type 2 diabetes and nephropathy.

Conclusions:

  • Diminished MMP-7 expression may contribute to fibronectin accumulation in diabetic nephropathy.
  • AGEs and/or TGF-beta likely play a role in reducing MMP-7 expression.
  • MMP-7 represents a potential therapeutic target for diabetic kidney disease.