Adipocyte-Derived Plasma Protein Adiponectin Acts as a Platelet-Derived Growth Factor-BB–Binding Protein and Regulates Growth Factor–Induced Common Postreceptor Signal in Vascular Smooth Muscle Cell

DOI Web Site 被引用文献57件
  • Yukio Arita
    From the Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka and First Institute of New Drug Research (M.M., Y. Ohmoto), Otsuka Pharmaceutical Co, Ltd, Tokushima, Japan.
  • Shinji Kihara
    From the Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka and First Institute of New Drug Research (M.M., Y. Ohmoto), Otsuka Pharmaceutical Co, Ltd, Tokushima, Japan.
  • Noriyuki Ouchi
    From the Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka and First Institute of New Drug Research (M.M., Y. Ohmoto), Otsuka Pharmaceutical Co, Ltd, Tokushima, Japan.
  • Kazuhisa Maeda
    From the Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka and First Institute of New Drug Research (M.M., Y. Ohmoto), Otsuka Pharmaceutical Co, Ltd, Tokushima, Japan.
  • Hiroshi Kuriyama
    From the Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka and First Institute of New Drug Research (M.M., Y. Ohmoto), Otsuka Pharmaceutical Co, Ltd, Tokushima, Japan.
  • Yoshihisa Okamoto
    From the Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka and First Institute of New Drug Research (M.M., Y. Ohmoto), Otsuka Pharmaceutical Co, Ltd, Tokushima, Japan.
  • Masahiro Kumada
    From the Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka and First Institute of New Drug Research (M.M., Y. Ohmoto), Otsuka Pharmaceutical Co, Ltd, Tokushima, Japan.
  • Kikuko Hotta
    From the Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka and First Institute of New Drug Research (M.M., Y. Ohmoto), Otsuka Pharmaceutical Co, Ltd, Tokushima, Japan.
  • Makoto Nishida
    From the Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka and First Institute of New Drug Research (M.M., Y. Ohmoto), Otsuka Pharmaceutical Co, Ltd, Tokushima, Japan.
  • Masahiko Takahashi
    From the Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka and First Institute of New Drug Research (M.M., Y. Ohmoto), Otsuka Pharmaceutical Co, Ltd, Tokushima, Japan.
  • Tadashi Nakamura
    From the Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka and First Institute of New Drug Research (M.M., Y. Ohmoto), Otsuka Pharmaceutical Co, Ltd, Tokushima, Japan.
  • Iichiro Shimomura
    From the Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka and First Institute of New Drug Research (M.M., Y. Ohmoto), Otsuka Pharmaceutical Co, Ltd, Tokushima, Japan.
  • Masahiro Muraguchi
    From the Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka and First Institute of New Drug Research (M.M., Y. Ohmoto), Otsuka Pharmaceutical Co, Ltd, Tokushima, Japan.
  • Yasukazu Ohmoto
    From the Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka and First Institute of New Drug Research (M.M., Y. Ohmoto), Otsuka Pharmaceutical Co, Ltd, Tokushima, Japan.
  • Tohru Funahashi
    From the Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka and First Institute of New Drug Research (M.M., Y. Ohmoto), Otsuka Pharmaceutical Co, Ltd, Tokushima, Japan.
  • Yuji Matsuzawa
    From the Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka and First Institute of New Drug Research (M.M., Y. Ohmoto), Otsuka Pharmaceutical Co, Ltd, Tokushima, Japan.

抄録

<jats:p> <jats:bold> <jats:italic> <jats:bold> <jats:italic>Background</jats:italic> — </jats:bold> </jats:italic> </jats:bold> Vascular smooth muscle cell proliferation plays an important role in the development of atherosclerosis. We previously reported that adiponectin, an adipocyte-specific plasma protein, accumulated in the human injured artery and suppressed endothelial inflammatory response as well as macrophage-to-foam cell transformation. The present study investigated the effects of adiponectin on proliferation and migration of human aortic smooth muscle cells (HASMCs). </jats:p> <jats:p> <jats:bold> <jats:italic> <jats:bold> <jats:italic>Methods and Results</jats:italic> — </jats:bold> </jats:italic> </jats:bold> HASMC proliferation was estimated by [ <jats:sup>3</jats:sup> H] thymidine uptake and cell number. Cell migration assay was performed using a Boyden chamber. Physiological concentrations of adiponectin significantly suppressed both proliferation and migration of HASMCs stimulated with platelet-derived growth factor (PDGF)-BB. Adiponectin specifically bound to <jats:sup>125</jats:sup> I-PDGF-BB and significantly inhibited the association of <jats:sup>125</jats:sup> I-PDGF-BB with HASMCs, but no effects were observed on the binding of <jats:sup>125</jats:sup> I-PDGF-AA or <jats:sup>125</jats:sup> I-heparin–binding epidermal growth factor (EGF)–like growth factor (HB-EGF) to HASMCs. Adiponectin strongly and dose-dependently suppressed PDGF-BB–induced p42/44 extracellular signal–related kinase (ERK) phosphorylation and PDGF β-receptor autophosphorylation analyzed by immunoblot. Adiponectin also reduced PDGF-AA–stimulated or HB-EGF–stimulated ERK phosphorylation in a dose-dependent manner without affecting autophosphorylation of PDGF α-receptor or EGF receptor. </jats:p> <jats:p> <jats:bold> <jats:italic> <jats:bold> <jats:italic>Conclusions</jats:italic> — </jats:bold> </jats:italic> </jats:bold> The adipocyte-derived plasma protein adiponectin strongly suppressed HASMC proliferation and migration through direct binding with PDGF-BB and generally inhibited growth factor–stimulated ERK signal in HASMCs, suggesting that adiponectin acts as a modulator for vascular remodeling. </jats:p>

収録刊行物

  • Circulation

    Circulation 105 (24), 2893-2898, 2002-06-18

    Ovid Technologies (Wolters Kluwer Health)

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