FGF-2 signaling induces downregulation of TAZ protein in osteoblastic MC3T3-E1 cells

被引:27
作者
Eda, Homare [1 ,2 ]
Aoki, Katsuhiko [1 ]
Marumo, Keishi [2 ]
Fujii, Katsuyuki [2 ]
Ohkawa, Kiyoshi [1 ]
机构
[1] Jikei Univ, Sch Med, Dept Biochem, Minato Ku, Tokyo 1058461, Japan
[2] Jikei Univ, Sch Med, Dept Orthopaed Surg, Minato Ku, Tokyo 1058461, Japan
关键词
TAZ; fibroblast growth factor-2; osteoblast differentiation; MAP kinase signaling;
D O I
10.1016/j.bbrc.2007.11.140
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 [生物化学与分子生物学]; 081704 [应用化学];
摘要
Transcriptional coactivator with PDZ-binding motif (TAZ) protein is a coactivator of Runx2 and corepressor of PPAR gamma. It also induces differentiation of mesenchymal cells into osteoblasts. In this study, we found that FGF-2, which inhibits bone mineralization and stimulates cell proliferation, reduced the TAZ protein expression level in osteoblast-like cells, MC3T3-E1. This reduction was recovered by removing FGF-2 from the culture medium, which also restored the osteoblastic features of MC3T3-E1 cells. Furthermore, FGF2-induced reduction of TAZ is blocked by a SAPK/JNK-specific inhibitor. These findings suggest that the expression of TAZ protein is involved in osteoblast proliferation and differentiation. This may help elucidate the discrepancies in the effect of FGF-2 and contribute to the understanding of FGF/FGFR-associated craniosynostosis syndrome etiology and treatment. (c) 2007 Elsevier Inc. All rights reserved.
引用
收藏
页码:471 / 475
页数:5
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