Upregulation of Heme Oxygenase-1 in an Animal Model of Takotsubo Cardiomyopathy

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Author(s)

    • UEYAMA Takashi
    • Department of Anatomy and Cell Biology, Wakayama Medical University School of Medicine
    • KAWABE Tetsuya
    • Center for Educational Research and Development, Wakayama Medical University School of Medicine
    • HANO Takuzo
    • Center for Educational Research and Development, Wakayama Medical University School of Medicine
    • TSURUO Yoshihiro
    • Department of Anatomy and Cell Biology, Wakayama Medical University School of Medicine
    • UEDA Kazuki
    • Second Department of Internal Medicine, Wakayama Medical University School of Medicine
    • ICHINOSE Masao
    • Second Department of Internal Medicine, Wakayama Medical University School of Medicine
    • KIMURA Hiroko
    • Department of Forensic Medicine, Juntendo University School of Medicine
    • YOSHIDA Ken-ichi
    • Department of Legal Medicine, Graduate School of Medicine, University of Tokyo

Abstract

<b><i>Background:</i></b> Disturbance of the coronary microcirculation and catecholamine intoxication, which may be responsible for the pathogenesis of takotsubo cardiomyopathy, could trigger an oxidative stress response in the heart. <b><i>Methods and Results:</i></b> Expression and localization of inducible heme oxygenase-1 (HO-1), which is an oxidative stress-related factor in the heart of immobilization stressed (IMO) rats, an animal model of takotsubo cardiomyopathy, were investigated by real-time reverse transcriptase-polymerase chain reaction and in situ hybridization histochemistry and immunohistochemistry. In response to IMO, the levels of HO-1 mRNA in the heart and in the aorta were slightly increased at 90 min, and increased 3-fold at 3 h compared with control levels. The signals for HO-1 mRNA were expressed on scatted cells in the myocardium and aortic adventitia. Double fluorescence immunohistochemistry showed that HO-1 immunoreactive cells were also ED1 and ED2 positive, indicating that they were macrophages. The numbers of ED1 and ED2 positive cells were constant, whereas the number of HO-1 positive cells was increased 5-fold at 6 h compared with control levels. Blocking of α- and β-adrenoceptors attenuated IMO-induced upregulation of HO-1 mRNA levels in the heart. <b><i>Conclusions:</i></b> Emotional stress and a surge of catecholamine upregulate HO-1 in the cardiac and aortic macrophages. (<i>Circ J</i> 2009; <b>73:</b> 1141-1146)<br>

Journal

  • Circulation Journal

    Circulation Journal 73(6), 1141-1146, 2009-05-20

    The Japanese Circulation Society

References:  30

Cited by:  4

Codes

  • NII Article ID (NAID)
    10025931795
  • NII NACSIS-CAT ID (NCID)
    AA11591968
  • Text Lang
    ENG
  • Article Type
    Journal Article
  • ISSN
    13469843
  • Data Source
    CJP  CJPref  J-STAGE 
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