Smad7 gene transfer inhibits peritoneal fibrosis

Kidney Int. 2007 Dec;72(11):1336-44. doi: 10.1038/sj.ki.5002533. Epub 2007 Sep 12.

Abstract

Fibrosis mediated by transforming growth factor-beta (TGF-beta) is a common cause of peritoneal dialysis (PD) failure. In a model of peritoneal fibrosis, we tested the effect of Smad7, an inhibitor of TGF-beta signaling, using an ultrasound-microbubble-mediated delivery system. Rats were given daily PD for 4 weeks and received Smad7 or control plasmid transfer. The ultrasound technique enhanced Smad7 expression in a dose-dependent manner in more than 80% of the peritoneal cells after 3 days. The expression decreased by 14 days, but this was corrected by a second gene transfer. The overexpression of Smad7 substantially inhibited Smad2/3 activation, TGF-beta, plasminogen activator inhibitor-1, extracellular matrix, and myofibroblast mRNA, and protein expression in the peritoneal cells. The decreased peritoneal injury included the rise of mass transfer of glucose, a reduction of the ultrafiltration rate, and fibrotic thickening. Our studies suggest that ultrasound-mediated Smad7 gene delivery may be useful in the prevention or treatment of dialysis-induced peritoneal fibrosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cells, Cultured
  • Disease Models, Animal
  • Epithelium / metabolism
  • Epithelium / pathology
  • Fibrosis / etiology
  • Fibrosis / pathology
  • Fibrosis / prevention & control*
  • Gene Transfer Techniques
  • Male
  • Peritoneal Dialysis / adverse effects
  • Peritoneum / metabolism
  • Peritoneum / pathology*
  • Plasminogen Activator Inhibitor 1 / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Smad2 Protein / metabolism
  • Smad7 Protein / genetics*
  • Smad7 Protein / metabolism*
  • Transforming Growth Factor beta / metabolism

Substances

  • Plasminogen Activator Inhibitor 1
  • Smad2 Protein
  • Smad2 protein, rat
  • Smad7 Protein
  • Smad7 protein, rat
  • Transforming Growth Factor beta