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Down-regulation of glomerular matrix metalloproteinase-2 gene in human NIDDM

D Del Prete1, F Anglani, M Forino

  • 1Institute of Internal Medicine, University of Padova, Italy.

Diabetologia
|February 3, 1998
PubMed

Insights

In diabetic nephropathy, the MMP2 gene is down-regulated in glomeruli, unlike TIMP2. This MMP2 gene down-regulation is specific to diabetes and not a marker of kidney damage severity.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Diabetology

Background:

  • Mesangial matrix deposition regulation involves synthesis and degradation.
  • Matrix metalloproteinases (MMP) and tissue inhibitors of matrix metalloproteinases (TIMP) are key in matrix degradation.
  • Diabetic nephropathy is associated with inhibited mesangial matrix degradation.

Purpose of the Study:

  • To investigate the gene expression of MMP2 and TIMP2 in human diabetic nephropathy.
  • To determine if MMP2 gene down-regulation is a marker of diabetic nephropathy progression.

Main Methods:

  • Reverse transcription polymerase chain reaction (RT-PCR) on microdissected glomeruli and tubulo-interstitium.
  • Analysis of kidney biopsies from 16 NIDDM patients, 5 other kidney disease patients, and 5 controls.
  • Correlation with albumin excretion rate and renal histology in NIDDM patients.

Main Results:

  • TIMP2 was expressed in both glomeruli and tubulo-interstitium across all groups.
  • MMP2 gene was significantly down-regulated in glomeruli of all NIDDM patients.
  • MMP2 gene expression was present in control and other kidney disease groups, but not in NIDDM glomeruli.
  • MMP2 down-regulation was independent of albuminuria and renal histology in NIDDM patients.

Conclusions:

  • MMP2 gene is consistently down-regulated in the glomeruli of NIDDM patients.
  • The MMP2/TIMP2 expression pattern is distinctive in NIDDM.
  • MMP2 gene down-regulation appears to be a consequence of diabetes itself, not a specific marker for nephropathy severity.

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