TY - JOUR
T1 - STAT3-mediated astrocyte differentiation from mouse fetal neuroepithelial cells by mouse oncostatin M
AU - Yanagisawa, Makoto
AU - Nakashima, Kinichi
AU - Taga, Tetsuya
N1 - Funding Information:
We wish to thank Drs. T. Hara and A. Miyajima for mOSM, Dr. K. Ikenaka for GFAP promoter-containing reporter construct, Drs. K. Shimozaki and S. Nagata for pEF-Rluc, Drs. M. Minami and S. Akira for DN-STAT3-expressing construct, and Dr. T. Hisatsune for valuable discussion on neuroepithelial cell culture. We are very much grateful to Ms. Y. Nakamura for her excellent secretarial assistance. We also thank Ms. K. Saito for technical help. This work has been supported by a grant-in-aid from the Ministry of Education, Science, Sports and Culture of Japan, Human Frontier Science Program, Cell Science Research Foundation, Kowa Life Science Foundation, Japan Brain Foundation, Aksuko Ouchi Memorial Fund and Cell Fate Modulation Research Unit of Medical Research Institute in Tokyo Medical and Dental University.
PY - 1999/7/16
Y1 - 1999/7/16
N2 - The interleukin (IL)-6 family of cytokines share gp130 as a signal- transducing receptor component. We here show that oncostatin M (OSM), a member of this family, and its receptor components were expressed in embryonic mouse brain and that OSM induced astrocytes in cultured fetal mouse neuroepithelial cells. OSM induced promoter activation of the gene for an astrocyte marker, glial fibrillary acidic protein. The activation was completely blocked by expression of a dominant negative form of STAT3, a transcription factor activated downstream of gp130, or by introduction of a mutation in the STAT3 binding motif in the promoter. Taken together with its expression, we suggest that OSM contributes to the induction of astrocyte differentiation in a fetal developing brain via STAT3 activation.
AB - The interleukin (IL)-6 family of cytokines share gp130 as a signal- transducing receptor component. We here show that oncostatin M (OSM), a member of this family, and its receptor components were expressed in embryonic mouse brain and that OSM induced astrocytes in cultured fetal mouse neuroepithelial cells. OSM induced promoter activation of the gene for an astrocyte marker, glial fibrillary acidic protein. The activation was completely blocked by expression of a dominant negative form of STAT3, a transcription factor activated downstream of gp130, or by introduction of a mutation in the STAT3 binding motif in the promoter. Taken together with its expression, we suggest that OSM contributes to the induction of astrocyte differentiation in a fetal developing brain via STAT3 activation.
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U2 - 10.1016/S0304-3940(99)00447-4
DO - 10.1016/S0304-3940(99)00447-4
M3 - Article
C2 - 10454159
AN - SCOPUS:0033575426
SN - 0304-3940
VL - 269
SP - 169
EP - 172
JO - Neuroscience Letters
JF - Neuroscience Letters
IS - 3
ER -