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Smad mediates BMP‐2‐induced upregulation of FGF‐evoked PC12 cell differentiation
Author(s) -
Hayashi Hisaki,
Ishisaki Akira,
Imamura Toru
Publication year - 2003
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(03)00005-x
Subject(s) - downregulation and upregulation , smad , fibroblast growth factor , microbiology and biotechnology , bone morphogenetic protein 2 , bone morphogenetic protein , chemistry , fibroblast growth factor receptor , signal transduction , receptor , biology , biochemistry , in vitro , gene
We previously reported that bone morphogenetic protein (BMP)‐2 augments fibroblast growth factor (FGF)‐induced neuronal differentiation of PC12 cells by selectively upregulating FGF receptor (FGFR)‐1 expression. Here we describe the underlying mechanism. BMP‐2 activated Smad proteins in PC12 cells. Overexpression of Smad7 or Smad1, inhibitory and receptor‐regulated isoforms, respectively, suppressed or enhanced BMP‐2‐induced upregulation of FGFR‐1 expression. Smad 7 also inhibited the FGF‐induced PC12 differentiation. Our findings indicate that activation of a Smad signaling pathway is required for upregulation of FGFR‐1 expression by BMP‐2 and for the synergistic induction of PC12 differentiation by BMP‐2 and FGF.