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Osteoblast-Specific Expression of MEF Induces Osteopenia Through Downregulation of Osteoblastogenesis and Upregulation of Osteoclastogenesis

Cited 6 time in Web of Science Cited 6 time in Scopus
Authors
Seul, Keyung-Jo; Cho, Hye-Sim; Heo, Sun-Hee; Baek, Wook-Young; Park, Eui Kyun; Ryoo, Hyun-Mo; Cho, Je-Yoel; Choi, Je-Yong; Kim, Jung-Eun
Issue Date
2011-02
Publisher
WILEY-BLACKWELL
Citation
JOURNAL OF BONE AND MINERAL RESEARCH, Vol.26, No.2, pp.341-350
Keywords
MEF (MYELOID ELF-1-LIKE FACTOR)TRANSGENIC MICEBONE REMODELINGBONE FORMATIONCOL1 alpha 1 PROMOTER
Abstract
In bone remodeling, various transcriptional factors are involved, and the deficiency or overexpression of some of these factors results in bone defects. Myeloid elf-1-like factor (MEF) is one of the Ets transcription factors that control the expression of genes that are critical for biologic processes such as cell proliferation, differentiation, and death. Previously, we reported that MEF promotes cell proliferation and functions as a negative regulator of osteogenic differentiation by interacting directly with Runx2 and suppressing its transcriptional activity. To investigate the in vivo function of MEF in bone formation and bone remodeling in vivo, we generated transgenic mice that overexpress MEF in osteoblasts under the control of the 2.3-kb Col1 alpha 1 promoter, named Col1 alpha 1-MEF. Femoral bone in Col1 alpha 1-MEF transgenic mice exhibited low bone mass with fewer trabecular bones and thinner and less developed cortical bones. The mineralized volume fraction (BV/TV) and bone- forming rate (BFR) were remarkably decreased to about 63% and 40%, respectively, in 6-week-old MEF transgenic mice compared with wild-type mice. In addition, reduced bone mineral density was observed in lumbar vertebrae of Col1 alpha 1-MEF transgenic mice. The number of TRACP(+) osteoclasts was increased in Col1 alpha 1-MEF transgenic mice and MEF-overexpressing MC3T3-E1 cells. All these in vivo results suggest that MEF suppresses bone formation by osteoblasts and facilitates bone resorption by activating osteoclasts indirectly. (C) 2011 American Society for Bone and Mineral Research.
ISSN
0884-0431
Language
English
URI
https://hdl.handle.net/10371/80555
DOI
https://doi.org/10.1002/jbmr.208
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College of Dentistry/School of Dentistry (치과대학/치의학대학원)Dept. of Dentistry (치의학과)Journal Papers (저널논문_치의학과)
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