TY - JOUR
T1 - Cardiotrophin-like cytokine induces astrocyte differentiation of fetal neuroepithelial cells via activation of STAT3
AU - Uemura, Atsumi
AU - Takizawa, Takumi
AU - Ochiai, Wataru
AU - Yanagisawa, Makoto
AU - Nakashima, Kinichi
AU - Taga, Tetsuya
N1 - Funding Information:
We thank Dr Giorgio Senaldi, Amgen Inc. for providing CLC/NNT-1/BSF-3, Yamanouchi Pharmaceutical Co., Ltd. for BMP2, and Drs Shigekazu Nagata and Koji Shimozaki for pEF-Rluc. We are very much grateful to Ms Yuki Noguchi for her excellent secretarial assistance. We also thank Ms Kaori Kaneko for technical help. This work was supported by Grant-in-Aid from Ministry of Education, Culture, Sports, Science and Technology, Takeda Science Foundation, and Human Frontier Science Program. M. Y. is supported by the Research Fellowships of the Japan Society for Promotion of Science for Young Scientists.
PY - 2002
Y1 - 2002
N2 - Cardiotrophin-like cytokine (CLC), also known as novel neurotrophin-1/B cell stimulating factor-3 (NNT-1/BSF-3), is a recently identified member of the interleukin (IL)-6 family of cytokines that share gp130 as a signal-transducing receptor component. In this study, we demonstrate that CLC is expressed in fetal mouse neuroepithelial cells and has a potential to induce their astrocyte differentiation in a synergistic manner with bone-morphogenetic protein (BMP)-2, which is also expressed in the fetal mouse brain. CLC-stimulation led to promoter activation of the gene for an astrocyte marker, glial fibrillary acidic protein (GFAP), which was clearly inhibited by expression of a dominant negative form of a transcription factor, STAT3, or by introduction of a mutation in a single STAT3-binding site in the promoter, suggesting a critical role of STAT3 in the CLC-induced GFAP transcription. These results suggest that CLC plays a role in astrocyte differentiation via STAT3 activation within the developing brain.
AB - Cardiotrophin-like cytokine (CLC), also known as novel neurotrophin-1/B cell stimulating factor-3 (NNT-1/BSF-3), is a recently identified member of the interleukin (IL)-6 family of cytokines that share gp130 as a signal-transducing receptor component. In this study, we demonstrate that CLC is expressed in fetal mouse neuroepithelial cells and has a potential to induce their astrocyte differentiation in a synergistic manner with bone-morphogenetic protein (BMP)-2, which is also expressed in the fetal mouse brain. CLC-stimulation led to promoter activation of the gene for an astrocyte marker, glial fibrillary acidic protein (GFAP), which was clearly inhibited by expression of a dominant negative form of a transcription factor, STAT3, or by introduction of a mutation in a single STAT3-binding site in the promoter, suggesting a critical role of STAT3 in the CLC-induced GFAP transcription. These results suggest that CLC plays a role in astrocyte differentiation via STAT3 activation within the developing brain.
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U2 - 10.1006/cyto.2002.1006
DO - 10.1006/cyto.2002.1006
M3 - Article
C2 - 12090754
AN - SCOPUS:0036020275
SN - 1043-4666
VL - 18
SP - 1
EP - 7
JO - Cytokine
JF - Cytokine
IS - 1
ER -