Hdl Handle:
http://hdl.handle.net/10675.2/543
Title:
Regulation of osteoclast function and bone mass by RAGE
Authors:
Zhou, Zheng; Immel, David; Xi, Cai-Xia; Bierhaus, Angelika; Feng, Xu; Mei, Lin; Nawroth, Peter; Stern, David M.; Xiong, Wen-Cheng
Abstract:
The receptor for advanced glycation end products (RAGE) is a member of the immunoglobulin superfamily that has multiple ligands and is implicated in the pathogenesis of various diseases, including diabetic complications, neurodegenerative disorders, and inflammatory responses. However, the role of RAGE in normal physiology is largely undefined. Here, we present evidence for a role of RAGE in osteoclast maturation and function, which has consequences for bone remodeling. Mice lacking RAGE had increased bone mass and bone mineral density and decreased bone resorptive activity in vivo. In vitroâ differentiated RAGE-deficient osteoclasts exhibited disrupted actin ring and sealing zone structures, impaired maturation, and reduced bone resorptive activity. Impaired signaling downstream of αvβ3 integrin was observed in RAGEâ /â bone marrow macrophages and precursors of OCs. These results demonstrate a role for RAGE in osteoclast actin cytoskeletal reorganization, adhesion, and function, and suggest that the osteosclerotic-like phenotype observed in RAGE knockout mice is due to a defect in osteoclast function.
Citation:
J Exp Med. 2006 Apr 17; 203(4):1067-1080
Issue Date:
17-Apr-2006
URI:
http://hdl.handle.net/10675.2/543
DOI:
10.1084/jem.20051947
PubMed ID:
16606672
PubMed Central ID:
PMC2118287
Type:
Article
ISSN:
1540-9538
Appears in Collections:
Institute of Molecular Medicine and Genetics: Faculty Research and Presentations

Full metadata record

DC FieldValue Language
dc.contributor.authorZhou, Zhengen_US
dc.contributor.authorImmel, Daviden_US
dc.contributor.authorXi, Cai-Xiaen_US
dc.contributor.authorBierhaus, Angelikaen_US
dc.contributor.authorFeng, Xuen_US
dc.contributor.authorMei, Linen_US
dc.contributor.authorNawroth, Peteren_US
dc.contributor.authorStern, David M.en_US
dc.contributor.authorXiong, Wen-Chengen_US
dc.date.accessioned2012-10-26T16:26:36Z-
dc.date.available2012-10-26T16:26:36Z-
dc.date.issued2006-04-17en_US
dc.identifier.citationJ Exp Med. 2006 Apr 17; 203(4):1067-1080en_US
dc.identifier.issn1540-9538en_US
dc.identifier.pmid16606672en_US
dc.identifier.doi10.1084/jem.20051947en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/543-
dc.description.abstractThe receptor for advanced glycation end products (RAGE) is a member of the immunoglobulin superfamily that has multiple ligands and is implicated in the pathogenesis of various diseases, including diabetic complications, neurodegenerative disorders, and inflammatory responses. However, the role of RAGE in normal physiology is largely undefined. Here, we present evidence for a role of RAGE in osteoclast maturation and function, which has consequences for bone remodeling. Mice lacking RAGE had increased bone mass and bone mineral density and decreased bone resorptive activity in vivo. In vitroâ differentiated RAGE-deficient osteoclasts exhibited disrupted actin ring and sealing zone structures, impaired maturation, and reduced bone resorptive activity. Impaired signaling downstream of αvβ3 integrin was observed in RAGEâ /â bone marrow macrophages and precursors of OCs. These results demonstrate a role for RAGE in osteoclast actin cytoskeletal reorganization, adhesion, and function, and suggest that the osteosclerotic-like phenotype observed in RAGE knockout mice is due to a defect in osteoclast function.en_US
dc.rightsCopyright © 2006, The Rockefeller University Pressen_US
dc.subjectArticlesen_US
dc.titleRegulation of osteoclast function and bone mass by RAGEen_US
dc.typeArticleen_US
dc.identifier.pmcidPMC2118287en_US
dc.contributor.corporatenameInstitute of Molecular Medicine and Genetics-
dc.contributor.corporatenameDepartment of Neurology-

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