Effect of Adiponectin on Cardiac Allograft Vasculopathy

DOI Web Site PubMed 参考文献52件
  • Ishihara Takashi
    Department of Cardiovascular Medicine, Tokyo Medical and Dental University
  • Haraguchi Go
    Department of Cardiovascular Medicine, Tokyo Medical and Dental University
  • Konishi Masanori
    Department of Cardiovascular Medicine, Tokyo Medical and Dental University
  • Ohigashi Hirokazu
    Department of Cardiovascular Medicine, Tokyo Medical and Dental University
  • Saito Kiyomi
    Department of Pharmacokinetics/Pharmacodynamics, School of Pharmacy, Showa University
  • Nakano Yasuko
    Department of Pharmacogenomics, School of Pharmacy, Showa University
  • Isobe Mitsuaki
    Department of Cardiovascular Medicine, Tokyo Medical and Dental University

この論文をさがす

抄録

Background: The role of adiponectin (APN), an adipose tissue-specific secretory protein, on chronic rejection after cardiac transplantation in APN-sense transgenic mice (APN-SE) was evaluated. Methods and Results: Heterotopic cardiac transplantation in major histocompatibility complex class II-mismatched mice was performed. B6.C-H-2bm12KhEg (Bm12) hearts were transplanted into APN-SE, and allografts were harvested at 8 weeks after transplantation. Quantitative polymerase chain reaction (PCR) and immunohistochemical staining showed that the expression of both AdipoR1 and AdipoR2 was induced in APN-SE recipients. Neointimal hyperplasia was significantly decreased in allografts transplanted into APN-SE (luminal occlusion, 8.9±2.2%) compared to those transplanted into controls (49.4±10.5%; P=0.011). APN-SE showed significantly reduced mRNA levels of interferon (IFN)-γ, tumor necrosis factor (TNF)-α, interleukin (IL)-2, IL-6, and monocyte chemoattractant protein-1 (MCP-1) by quantitative PCR. Western blot analysis revealed that the protein levels of IFN-γ and MCP-1 were reduced in APN-SE recipients. Proliferation of smooth muscle cells stimulated with activated T cells was suppressed by APN addition, and this effect was canceled by treatment with an adenosine monophosphate-activated protein kinase (AMPK) inhibitor. Conclusions: APN plays a critical role in the attenuation of chronic rejection by suppressing inflammatory cytokine and chemokine expression and enhancing APN receptor expression. APN plays a beneficial role in reducing the progression of cardiac allograft vasculopathy through the AMPK pathway. (Circ J 2011; 75: 2005-2012)<br>

収録刊行物

  • Circulation Journal

    Circulation Journal 75 (8), 2005-2012, 2011

    一般社団法人 日本循環器学会

参考文献 (52)*注記

もっと見る

関連プロジェクト

もっと見る

キーワード

詳細情報 詳細情報について

問題の指摘

ページトップへ