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Expression of fibroblast growth factor receptor-3 (FGFR3), signal transducer and activator of transcription-1, and cyclin-dependent kinase inhibitor p21 during endochondral ossification: differential role of FGFR3 in skeletal development and fracture repair.

Authors: Nakajima, A  Shimizu, S  Moriya, H  Yamazaki, M 
Citation: Nakajima A, etal., Endocrinology 2003 Oct;144(10):4659-68. Epub 2003 Jul 3.
Pubmed: (View Article at PubMed) PMID:12960068
DOI: Full-text: DOI:10.1210/en.2003-0158

Increasing evidence suggests that fibroblast growth factor receptor-3 (FGFR3) is a negative regulator of endochondral bone growth; however, its role during skeletal repair is unknown. Using a rat model of closed femoral fracture healing, we analyzed the spatial and temporal expression of FGFR3. To assess a possible role for FGFR3 during healing, we also analyzed the spatial and temporal expression of signal transducer and activator of transcription-1 (STAT1) and cyclin-dependent kinase inhibitor p21, important mediators of FGFR3 signaling. Before these experiments, we studied the spatial expression of FGFR3 during skeletal development in mouse embryos. At 16.5 and 19.5 d post coitum, FGFR3 mRNA was strongly expressed in resting and proliferating chondrocytes but weakly in hypertrophic chondrocytes and not in osteoblasts. In contrast, during fracture repair, it was strongly expressed in prehypertrophic chondrocytes, and the expression level reached a maximum on d 14. Immunoreactivity for STAT1 was detected in the cytoplasm of chondrocytes on d 4 and 7 and both in the cytoplasm and nucleus of hypertrophic chondrocytes on d 14. Furthermore, FGFR3, STAT1, and p21 exhibited a similar temporal expression profile, suggesting that FGFR3-mediated STAT1-p21 signaling plays a role in fracture repair. These results indicate a differential role of FGFR3 in skeletal development and fracture repair.

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RGD Object Information
RGD ID: 1299061
Created: 2004-06-01
Species: All species
Last Modified: 2006-04-25
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.