Receptor-mediated toxicity to pericytes of advanced glycosylation end products: a possible mechanism of pericyte loss in diabetic microangiopathy

Biochem Biophys Res Commun. 1995 Aug 15;213(2):681-7. doi: 10.1006/bbrc.1995.2185.


The influence of advanced glycosylation end products (AGE) on bovine retinal pericytes was investigated. When pericytes were cultured with AGE-bovine serum albumin (BSA), pericyte growth was significantly retarded in a dose-dependent manner. They also exhibited an immediate toxicity to pericytes. However, MRC-5 human fibroblasts were totally resistant to AGE-BSA. Moreover, antisense oligonucleotides complementary to mRNA coding for AGE receptor were found to reverse the AGE-induced decrease in viable pericyte number, although the mRNA level was about one order of magnitude lower in pericytes than in the fibroblasts. These results indicate that pericytes may possess a peculiar sensitivity to AGE, and that AGE ligand-receptor interactions may play an important role in the pathogenesis of pericyte loss, the principal change in diabetic microangiopathies.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Base Sequence
  • Cattle
  • Cell Division / drug effects
  • Cell Line
  • Cells, Cultured
  • Fibroblasts / drug effects
  • Glycation End Products, Advanced / toxicity*
  • Glycosylation
  • Humans
  • Molecular Sequence Data
  • Oligonucleotides, Antisense / pharmacology
  • RNA, Messenger / metabolism
  • Receptor for Advanced Glycation End Products
  • Receptors, Immunologic / antagonists & inhibitors
  • Receptors, Immunologic / genetics
  • Receptors, Immunologic / physiology*
  • Retina / drug effects*
  • Serum Albumin, Bovine / pharmacology


  • Glycation End Products, Advanced
  • Oligonucleotides, Antisense
  • RNA, Messenger
  • Receptor for Advanced Glycation End Products
  • Receptors, Immunologic
  • Serum Albumin, Bovine