부산대학교 도서관

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.bbrc.2009.09.123 Byline: Xiumin Lu (a)(b), Nan Su (a), Jing Yang (a), Wei Huang (b), Can Li (a), Ling Zhao (a), Qifen He (a), Xiaolan Du (a), Yue Shen (a), Bo Chen (a), Lin Chen (a) Keywords: FGFR1; Bone remodeling; Osteoclast; MAPK Abstract: To elucidate the direct role and mechanism of FGFR1 signaling in the differentiation and activation of osteoclasts, we conditionally inactivated FGFR1 in bone marrow monocytes and mature osteoclasts of mice. Mice deficient in FGFR1 (Fgfr1.sup.-/-) exhibited misregulated bone remodeling with reduced osteoclast number and impaired osteoclast function. In vitro assay demonstrated that the number of tartrate-resistant acid phosphatase (TRAP) positive osteoclasts derived from bone marrow monocytes of Fgfr1.sup.-/- mice was significantly diminished. The bone resorption activity of mature osteoclasts derived from Fgfr1.sup.-/- mice was also suppressed. Further analysis showed that the osteoclasts with FGFR1 deficiency exhibited downregulated expression of genes related to osteoclastic activity including TRAP and MMP-9. The phosphorylation of Erk1/2 mitogen-activated protein (MAP) kinase was also decreased. Our results suggest that FGFR1 is indispensable for complete differentiation and activation of osteoclasts in mice. Author Affiliation: (a) State Key Laboratory of Trauma, Burns and Combined Injury, Trauma Center, Institute of Surgery Research, Daping Hospital, Third Military Medical University, Chongqing 400042, China (b) School of Chemical and Biological Engineering, Chongqing University of Technology, Chongqing 400050, China Article History: Received 3 September 2009