Smad mediates BMP‐2‐induced upregulation of FGF‐evoked PC12 cell differentiation

FEBS Letters

Imamura, Toru¹  Ishisaki, Akira¹  Hayashi, Hisaki¹ 

[1] Age Dimension Research Center, National Institute of Advanced Industrial Science and Technology (AIST), Tsukuba, Ibaraki 305-8566, Japan

关键词: Smad;    Bone morphogenetic protein-2;    Fibrobast growth factor;    Fibrobast growth factor receptor type-1;    PC12 cells;    BMP;    bone morphogenetic protein;    FGF;    fibroblast growth factor;    FGFR;    FGF receptor;    GAPDH;    glyceraldehyde 3-phosphate dehydrogenase;    MAPK;    mitogen-activated protein kinase;    RT-PCR;    reverse-transcription-polymerase chain reaction;    TGF-β;    transforming growth factor-β;   

DOI  :  10.1016/S0014-5793(03)00005-X

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

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.

【 授权许可】

Unknown