Runx2 induces osteoblast and chondrocyte differentiation and enhances their migration by coupling with PI3K-Akt signaling.
Runx2 induces osteoblast and chondrocyte differentiation and enhances their migration by coupling with PI3K-Akt signaling.
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DOI:
10.1083/jcb.200401138
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发表时间:
2004-07-05
期刊:
影响因子:
--
通讯作者:
Komori T
中科院分区:
文献类型:
--
作者:
Fujita T;Azuma Y;Fukuyama R;Hattori Y;Yoshida C;Koida M;Ogita K;Komori T
Runx2 and phosphatidylinositol 3-kinase (PI3K)–Akt signaling play important roles in osteoblast and chondrocyte differentiation. We investigated the relationship between Runx2 and PI3K-Akt signaling. Forced expression of Runx2 enhanced osteoblastic differentiation of C3H10T1/2 and MC3T3-E1 cells and enhanced chondrogenic differentiation of ATDC5 cells, whereas these effects were blocked by treatment with IGF-I antibody or LY294002 or adenoviral introduction of dominant-negative (dn)–Akt. Forced expression of Runx2 or dn-Runx2 enhanced or inhibited cell migration, respectively, whereas the enhancement by Runx2 was abolished by treatment with LY294002 or adenoviral introduction of dn-Akt. Runx2 up-regulated PI3K subunits (p85 and p110β) and Akt, and their expression patterns were similar to that of Runx2 in growth plates. Treatment with LY294002 or introduction of dn-Akt severely diminished DNA binding of Runx2 and Runx2-dependent transcription, whereas forced expression of myrAkt enhanced them. These findings demonstrate that Runx2 and PI3K-Akt signaling are mutually dependent on each other in the regulation of osteoblast and chondrocyte differentiation and their migration.
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影响因子:
64.5
作者:
Nakashima, K;Zhou, X;de Crombrugghe, B
通讯作者:
de Crombrugghe, B
DOI:
10.1016/j.bbrc.2004.01.104
发表时间:
2004-03-12
影响因子:
3.1
作者:
Fukuyama, R;Fujita, T;Komori, T
通讯作者:
Komori, T
影响因子:
64.5
作者:
Ducy, P;Zhang, R;Karsenty, G
通讯作者:
Karsenty, G
影响因子:
15.9
作者:
Ogata, N;Chikazu, D;Kawaguchi, H
通讯作者:
Kawaguchi, H
DOI:
10.1083/jcb.200204046
发表时间:
2002-10-14
期刊:
The Journal of cell biology
影响因子:
--
作者:
Akune T;Ogata N;Hoshi K;Kubota N;Terauchi Y;Tobe K;Takagi H;Azuma Y;Kadowaki T;Nakamura K;Kawaguchi H
通讯作者:
Kawaguchi H