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J. Biol. Chem., Vol. 277, Issue 51, 50112-50120, December 20, 2002
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From the Department of Dental and Medical Biochemistry, Hiroshima
University Graduate School of Biomedical Sciences, Hiroshima 734-8553, Japan, the § Institute for Frontier Medical Sciences, Jilin
University, Changchun 130021, China, and the ¶ Department of
Orthopeadics Surgery, Jikei University School of Medicine, Minato,
Tokyo 105, Japan
The mRNA level of basic helix-loop-helix
transcription factor DEC1 (BHLHB2)/Stra13/Sharp2 was up-regulated
during chondrocyte differentiation in cultures of ATDC5 cells and
growth plate chondrocytes, and in growth plate cartilage in
vivo. Forced expression of DEC1 in ATDC5 cells induced
chondrogenic differentiation, and insulin increased this effect of DEC1
overexpression. Parathyroid hormone (PTH) and PTH-related peptide
(PTHrP) suppressed DEC1 expression and the differentiation of ATDC5
cells, but DEC1 overexpression antagonized this inhibitory action of
PTH/PTHrP. Transforming growth factor-
Basic Helix-loop-helix Protein DEC1 Promotes Chondrocyte
Differentiation at the Early and Terminal Stages*
,,
or bone morphogenetic
protein-2, as well as insulin, induced DEC1 expression in ATDC5
cultures where it induced chondrogenic differentiation. In pellet
cultures of bone marrow mesenchymal stem cells exposed to transforming
growth factor- and insulin, DEC1 was induced at the earliest stage
of chondrocyte differentiation and also at the hypertrophic stage.
Overexpression of DEC1 in the mesenchymal cells induced the mRNA
expressions of type II collagen, Indian hedgehog, and Runx2, as well as
cartilage matrix accumulation; overexpression of DEC1 in growth plate
chondrocytes at the prehypertrophic stage increased the mRNA levels
of Indian hedgehog, Runx2, and type X collagen, and also increased
alkaline phosphatase activity and mineralization. To our
knowledge, DEC1 is the first transcription factor that can
promote both chondrogenic differentiation and terminal differentiation.
*
This work was supported by a grant-in-aid for science from
the Ministry of Education, Science, Sports and Culture of Japan.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Both authors contributed equally to this study.
To whom correspondence should be addressed. Fax:
81-82-257-5629; E-mail: ykato@hiroshima-u.ac.jp.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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