Disordered osteoclast formation in RAGE-deficient mouse establishes an essential role for RAGE in diabetes related bone loss

Kehong Ding, Zai Zhao Wang, Mark W Hamrick, Zhong Bin Deng, Li Zhou, Baolin Kang, Sheng Li Yan, Jin-Xiong She, David M. Stern, Carlos M Isales, Qing Sheng Mi

Research output: Contribution to journalArticle

88 Scopus citations

Abstract

The mechanisms underlying diabetes-mediated bone loss are not well defined. It has been reported that the advanced glycation endproducts (AGEs) and receptor for AGEs (RAGEs) are involved in diabetic complications. Here, mice deficient in RAGE were used as a model for investigating the effects of RAGE on bone mass. We found that RAGE-/- mice have a significantly increased bone mass and bone biomechanical strength and a decreased number of osteoclasts compared to wild-type mice. The serum levels of IL-6 and bone breakdown marker pyridinoline were significantly decreased in RAGE-/- mice. RAGE -/- mice maintain bone mass following ovariectomy, whereas wild-type mice lose bone mass. Furthermore, osteoclast-like cells do express RAGE mRNA. Our data therefore indicate that RAGE serves as a positive factor to regulate the osteoclast formation, directly implicates a role for RAGE in diabetes-promoted bone destruction, and documents that the AGE-RAGE interaction may account for diabetes associated bone loss.

Original languageEnglish (US)
Pages (from-to)1091-1097
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume340
Issue number4
DOIs
StatePublished - Feb 24 2006

Keywords

  • Bone
  • Diabetes
  • Knockout
  • Osteoclast
  • Receptor for advanced glycation endproducts

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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