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J. Biol. Chem., Vol. 279, Issue 51, 53848-53856, December 17, 2004

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Epidermal Growth Factor Receptor-deficient Mice Have Delayed Primary Endochondral Ossification Because of Defective Osteoclast Recruitment^*

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

From the Departments of Medicine and ^¶Anatomy, and Lung Biology Center, University of California, San Francisco, California 94143

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. Ossification of the growth plates was also abnormal resulting in an expanded area of growth plate hypertrophic cartilage and few bony trabeculae. The delayed osteoclast recruitment was not because of inadequate expression of matrix metalloproteinases, including matrix metalloproteinase-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.

Received for publication, March 19, 2004 , and in revised form, September 8, 2004.

^* This work was supported by National Institutes of Health Grant AR46238 (to T. H. V. and Z. W.) and a grant from the Sandler Family Supporting Foundation (to T. H. V.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

^|| To whom correspondence should be addressed: Box 2911, University of California, San Francisco, CA 94143-2911. Tel.: 415-514-4266; Fax: 415-514-4365; E-mail: thiennu{at}itsa.ucsf.edu.

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