Regulation of advanced glycation end product (AGE) receptors and apoptosis by AGEs in osteoblast-like cells

Mol Cell Biochem. 2007 Dec;306(1-2):87-94. doi: 10.1007/s11010-007-9557-8. Epub 2007 Jul 28.

Abstract

Advanced glycation end products (AGEs) have been proposed as the pathological mechanisms underlying diabetic chronic complications. They may also play a role in the pathogenesis of diabetic osteopenia, although their mechanisms of action remain unclear. We investigated the protein (immunofluorescence) and gene expression (realtime RT-PCR) of two receptors for AGEs, RAGE and galectin-3, as well as their regulation by AGEs, and the apoptotic effect on osteoblast-like cells (UMR106 and MC3T3E1) in culture. AGEs up-regulated the expression of RAGE and galectin-3 in both cells lines. These effects were accompanied by an increase in the corresponding mRNA in the non-tumoral MC3T3E1 but not in the osteosarcoma UMR106 cells. Finally, we demonstrated that a 24 h exposure to AGEs induced apoptosis in both cell lines. Thus, AGEs-receptors may play important roles in the bone alterations described in aging and diabetic patients.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis*
  • Cell Differentiation
  • Cells, Cultured
  • Fluorescent Antibody Technique
  • Galectin 3 / genetics
  • Galectin 3 / metabolism
  • Glycation End Products, Advanced / pharmacology*
  • Mice
  • Osteoblasts / drug effects*
  • Osteoblasts / metabolism
  • Receptor for Advanced Glycation End Products
  • Receptors, Immunologic / genetics
  • Receptors, Immunologic / metabolism*
  • Reverse Transcriptase Polymerase Chain Reaction

Substances

  • Galectin 3
  • Glycation End Products, Advanced
  • Receptor for Advanced Glycation End Products
  • Receptors, Immunologic