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Glomerular expression of connective tissue growth factor mRNA in various renal diseases

Daisuke Suzuki1, Masao Toyoda, Tomoya Umezono

  • 1Division of Nephrology and Metabolism, Department of Internal Medicine, School of Medicine, Tokai University, Isehara, Kanagawa, Japan. daisuke@is.icc.u-tokyo.ac.jp

Nephrology (Carlton, Vic.)
|March 12, 2004
PubMed

Insights

Connective tissue growth factor (CTGF) is elevated in diabetic nephropathy and IgA nephropathy, suggesting its role in glomerulosclerosis progression. This finding highlights CTGF as a potential factor in these kidney diseases.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Pathogenesis of Kidney Disease

Background:

  • Connective tissue growth factor (CTGF) is implicated in mesangial matrix accumulation and glomerulosclerosis.
  • Understanding CTGF's role in various nephropathies is crucial for identifying disease mechanisms.

Purpose of the Study:

  • To investigate the expression and localization of CTGF mRNA in different kidney diseases.
  • To elucidate the specific role of CTGF in diabetic nephropathy (DN), IgA nephropathy (IgA-N), membranous nephropathy (MN), and minimal change nephrotic syndrome (MCNS).

Main Methods:

  • In situ hybridization was used to evaluate CTGF mRNA expression in renal tissue samples.
  • Samples included patients with DN, IgA-N, MN, MCNS, and normal human kidney (NHK).
  • Quantification involved counting CTGF mRNA-positive cells in glomeruli as a percentage of total glomerular cells.

Main Results:

  • CTGF mRNA was primarily expressed in glomerular mesangial and epithelial cells.
  • Significantly higher CTGF mRNA expression was observed in DN and IgA-N compared to MN, MCNS, and NHK.
  • No significant difference in CTGF mRNA expression was found between DN and IgA-N.

Conclusions:

  • CTGF plays a significant role in the development and progression of glomerulosclerosis in DN and IgA-N.
  • Mesangial matrix expansion in DN and IgA-N is associated with elevated CTGF levels.
  • CTGF is implicated as a key factor in two major causes of end-stage renal failure.

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