title: Effects of new peritoneal dialysis solutions, pyridoxamine and AT1 receptor blocker, on TGF-beta1 and VEGF expression in rat peritoneal mesothelial cells.
abstract: BACKGROUND
  Transforming growth factor beta1 (TGF-beta1) and vascular endothelial growth factor (VEGF) are involved in peritoneal deterioration in continuous ambulatory peritoneal dialysis. The present study was designed to determine whether new peritoneal dialysis solutions (PDS), pyridoxamine (advanced glycation end products (AGE) inhibitor) or AT1 receptor blocker (ARB), affect the expression of VEGF and TGF-beta1 in rat peritoneal mesothelial cells (RPMC).
  
  
  METHODS
  RPMC were stimulated by phosphate-buffered saline (PBS) as control, Dianeal 1.5% (D 1.5%), Dianeal 2.5% (D 2.5%), Dianeal 4.25% (D 4.25%), Dianeal N 1.5% (N 1.5%), Dianeal N 2.5% (N 2.5%) or Extraneal (Ex). In co-incubation experiments, RPMC were stimulated with N 2.5% including pyridoxamine or olmesartan (ARB). VEGF and TGF-beta1 protein and mRNA expression in RPMC were analyzed by ELISA and RT-PCR.
  
  
  RESULTS
  Glucose-containing PDS, even N 2.5% diluted twofold with M199 (which contains 1.25% glucose), increased VEGF and TGF-beta1 expression in RPMC (p < 0.05). Ex did not inhibit VEGF expression and did not inhibit TGF- beta1 expression after 24 h in RPMC. Pyridoxamine and ARB significantly reduced N 2.5%-induced VEGF and TGF-beta1 protein and mRNA expression in RPMC (p < 0.01).
  
  
  CONCLUSIONS
  Neither new pH-neutral, lactate-buffered, low-GDP, two-chamber bag PDS, nor 7.5% icodextrin PDS alone satisfactorily inhibited VEGF and TGF-beta1 overproduction in RPMC, but ARB or pyridoxamine effectively inhibited glucose-containing PDS (N 2.5%)-induced overproduction.
authors: Department of Nephrology, Toho University School of Medicine, Tokyo, Japan. sm210@med.toho-u.ac.jp
authors: Sonoo
authors: S
authors: Mizuiri
authors: Yasushi
authors: Y
authors: Ohashi
authors: Hiromichi
authors: H
authors: Hemmi
authors: Michitsune
authors: M
authors: Arita
authors: Kanae
authors: K
authors: Yamada
authors: Toshiyuki
authors: T
authors: Aoki
authors: Moriatsu
authors: M
authors: Miyagi
authors: Ken
authors: K
authors: Sakai
authors: Atsushi
authors: A
authors: Aikawa
mesh_terms: D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology*; D000818:Animals; D002478:Cells, Cultured; D004847:Epithelial Cells / Q000187:drug effects* / Q000378:metabolism*; D015312:Hemodialysis Solutions; D008297:Male; D010530:Peritoneal Dialysis; D010537:Peritoneum / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism*; D011733:Pyridoxamine / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D053773:Transforming Growth Factor beta1 / Q000096:biosynthesis* / Q000187:drug effects*; D042461:Vascular Endothelial Growth Factor A / Q000096:biosynthesis* / Q000187:drug effects*
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D015312:Hemodialysis Solutions; D053773:Transforming Growth Factor beta1; D042461:Vascular Endothelial Growth Factor A; D011733:Pyridoxamine