Upregulation of endogenous heparin‐binding EGF‐like growth factor and its role as a survival factor in skeletal myotubes

FEBS Letters

Horikawa, Michiharu³  Nomura, Shintaro²  Higashiyama, Shigeki³  Ishikawa, Mutsuo¹  Kitamura, Yukihiko²  Taniguchi, Naoyuki³ 

[1] Department of Obstetrics and Gynecology, Asahikawa Medical College, 4-3-5-11, Nishikagura, Asahikawa, Hokkaido 078-8510, Japan;Department of Pathology, Osaka University Medical School, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan;Department of Biochemistry, Osaka University Medical School, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan

关键词: Heparin-binding EGF-like growth factor;    Epidermal growth factor receptor;    Cell survival;    Skeletal muscle;    C2C12;    Hypoxia;    EGF;    epidermal growth factor;    HB-EGF;    heparin-binding EGF-like growth factor;    proHB-EGF;    membrane-anchored heparin-binding EGF-like growth factor;    sHB-EGF;    soluble heparin-binding EGF-like growth factor;    EGFR;    epidermal growth factor receptor;   

DOI  :  10.1016/S0014-5793(99)01213-2

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

To investigate the role of heparin-binding EGF-like growth factor (HB-EGF) in skeletal muscle, we studied its function in skeletal myotubes in vitro using mouse C2C12 cells. Expression levels of membrane-anchored HB-EGF (proHB-EGF) protein were increased specifically during their differentiation among epidermal growth factor receptor (EGFR) ligands. Production levels of EGFR on the cell surface were constant. Tyrosine phosphorylation of EGFR, however, was constitutively increased during differentiation. Quenching of endogenous HB-EGF significantly rendered myotubes sensitive to apoptotic cell death induced by hypoxic stress, suggesting that proHB-EGF in the skeletal muscle is specifically upregulated to function as a survival factor.

【 授权许可】

Unknown