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Submitted on June 30, 2003
Accepted on September 25, 2003
1 Department of Materials Science and Engineering (H.Y.), Nagoya Institute of Technology, Gokiso-cyo, Showa-ku, Nagoya, 466-8555, Department of Animal Science (M.T.), Nippon Veterinary and Animal Science University 1-7-1 Kyonan-cho, Musashino, Tokyo 180-8602, Department of Biochemistry (N.N., N.N., K.N.) Faculty of Medicine, Mie University, 2-174 Edobashi, Tsu, Mie 514-8507, Japan
* To whom correspondence should be addressed. E-mail: h-yoshi{at}ks.kyy.nitech.ac.jp.
The signaling pathway of growth hormone (GH)-stimulated insulin-like growth factor I (IGF-I) gene expression is still unclear, although it has been reported that JAK-STAT5b pathway plays an important role in liver IGF-I expression. In this study, the GH-dependent IGF-I gene expression and its intracellular signaling mechanism have been examined in mouse pro-B, Ba/F3, cells stably expressing human GH receptor (Ba/F3-hGHR). The IGF-I gene expression was stimulated by human GH (0.01 
10 nM) in a dose-dependent fashion in Ba/F3-hGHR cells. The specific inhibitors for JAK2 remarkably suppressed the GH-induced IGF-I gene expression, but MAPK or PI3 kinase specific inhibitors failed to block the GH stimulation of the IGF-I gene expression. However, a non-specific tyrosine kinase inhibitor, genistein which dose not inhibit JAK2 and STAT5 phosphorylation significantly suppressed the GH-induced IGF-I gene expression. Additionally, a Ba/F3-hGHR mutant that contained the truncated C-terminal hGHR upto D351 showed no IGF-I gene expression in response to human GH. The D351 form normally has the GH-induced JAK/STAT5 tyrosine phosphorylation. These results suggest that JAK-STAT5 pathway, and novel tyrosine phosphorylation pathway depend on the signaling from the C-terminal region of hGHR would be involved in the GH-stimulated IGF-I gene expression in Ba/F3 cells.
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