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M403114200v1
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Papers In Press, published online ahead of print September 28, 2004
J. Biol. Chem, 10.1074/jbc.M403114200
Submitted on March 19, 2004
Revised on September 8, 2004
Accepted on September 28, 2004

EGFR-deficient mice have delayed primary endochondral ossification due to defective osteoclast recruitment

Ke Wang, Hiroaki Yamamoto, Jennie R. Chin, Zena Werb, and Thiennu H. Vu

Medicine, University of California, San Francisco, San Francisco, CA 94143-2911

Corresponding Author: thiennu{at}itsa.ucsf.edu

The epidermal growth factor receptor (EGFR) and its ligands function in diverse cellular functions including cell proliferation, differentiation, motility and survival. EGFR signaling is important for the development of many tissues, including skin, lungs, intestines, and the craniofacial skeleton. We have now determined the role of EGFR signaling in endochondral ossification. We analyzed long bone development in EGFR-deficient mice. EGFR deficiency caused delayed primary ossification of the cartilage anlage and delayed osteoclast and osteoblast recruitment. Secondary ossification was also abnormal resulting in an expanded area of growth plate hypertrophic cartilage and few bony trabeculae. The delayed osteoclast recruitment was not due to inadequate expression of matrix metalloproteinases, including MMP-9, which have previously been shown to be important for osteoclast recruitment. EGFR was expressed by osteoclasts, suggesting that EGFR ligands may act directly to affect the formation and/or function of these cells. EGFR signaling regulated osteoclast formation. Inhibition of EGFR tyrosine kinase activity decreased the generation of osteoclasts from cultured bone marrow cells.


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