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Runx2 determines bone maturity and turnover rate in postnatal bone development and is involved in bone loss in estrogen deficiency
Author(s) -
Maruyama Zenjiro,
Yoshida Carolina A.,
Furuichi Tatsuya,
Amizuka Norio,
Ito Masako,
Fukuyama Ryo,
Miyazaki Toshihiro,
Kitaura Hideki,
Nakamura Kouhei,
Fujita Takashi,
Kanatani Naoko,
Moriishi Takeshi,
Yamana Kei,
Liu Wenguang,
Kawaguchi Hiroshi,
Nakamura Kozo,
Komori Toshihisa
Publication year - 2007
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.21187
Subject(s) - runx2 , osteoblast , bone remodeling , biology , endocrinology , medicine , osteocalcin , bone cell , microbiology and biotechnology , alkaline phosphatase , genetics , biochemistry , in vitro , enzyme
Runx2 is an essential transcription factor for osteoblast differentiation. However, the functions of Runx2 in postnatal bone development remain to be clarified. Introduction of dominant‐negative (dn)‐ Runx2 did not inhibit Col1a1 and osteocalcin expression in mature osteoblastic cells. In transgenic mice that expressed dn‐ Runx2 in osteoblasts, the trabecular bone had increased mineralization, increased volume, and features of compact bone, and the expression of major bone matrix protein genes was relatively maintained. After ovariectomy, neither osteolysis nor bone formation was enhanced and bone was relatively conserved. In wild‐type mice, Runx2 was strongly expressed in immature osteoblasts but downregulated during osteoblast maturation. These findings indicate that the maturity and turnover rate of bone are determined by the level of functional Runx2 and Runx2 is responsible for bone loss in estrogen deficiency, but that Runx2 is not essential for maintenance of the expression of major bone matrix protein genes in postnatal bone development and maintenance. Developmental Dynamics 236:1876–1890, 2007. © 2007 Wiley‐Liss, Inc.