[Frontiers in Bioscience S3, 768-776, January 1, 2011]

RAGE and its ligands in bone metabolism

Zheng Zhou1, Wen-Cheng Xiong1

1Institute of Molecular Medicine and Genetics and Department of Neurology, Medical College of Georgia, Augusta, GA 30912

TABLE OF CONTENTS

1. Abstract
2. Introduction
3. Discussion
3.1. RAGE
3.1.1. RAGE & sRAGE in osteoclast activation
3.1.2. RAGE in osteoblasts and chondrocytes
3.2. HMGB1
3.2.1. HMGB1 expression and secretion in bone cells
3.2.2. HMGB1 functions in bone remodeling
3.2.3. HMGB1 expression and function in chondrocytes
3.3. AGE, S100, and APP/Abeta
3.3.1. AGE in bone remodeling
3.3.2. S100 in bone remodeling
3.3.3. Abeta in bone remodeling
4. Summary and Perspective
5. Acknowledgements
6. References

1. ABSTRACT

The receptor for advanced glycation end products (RAGE), a member of the immunoglobulin super-family transmembrane proteins, has multiple ligands, thus, is implicated in the pathogenesis of various diseases, including diabetic complications, neurodegenerative disorders, and inflammatory responses. Its function in normal physiology is beginning to be defined, and recent studies have pointed to an important role for RAGE and its ligands (e.g., HMGB1 (high mobility group box 1)) in innate immune response. In addition, RAGE and its ligands are also implicated in osteoclast activation and bone remodeling. Understanding how RAGE and its ligands regulate bone remodeling may provide insight into the pathogenesis of diabetes and chronic inflammation associated bone loss. Recent progress relevant to the functions of RAGE and its ligands in bone remodeling is discussed in this review.