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

• 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

Background: 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. Methods and Results: 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. Conclusions: Emotional stress and a surge of catecholamine upregulate HO-1 in the cardiac and aortic macrophages. (Circ J 2009; 73: 1141-1146)<br>

Journal

• Circulation Journal

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

  The Japanese Circulation Society

Keywords

• Catecholamines
• Emotional stress
• Oxidative stress

Details

• CRID: 1390001205103978368
• NII Article ID: 10025931795
• NII Book ID: AA11591968
• DOI: 10.1253/circj.cj-08-0988
• ISSN: 13474820
• ISSN: 13469843
• Web Site: http://www.jstage.jst.go.jp/article/circj/73/6/73_CJ-08-0988/_pdf
• Web Site: https://search.jamas.or.jp/link/ui/2009270145
• Text Lang: en
• Data Source:
  • JaLC
  • Crossref
  • CiNii Articles
  • KAKEN
• Abstract License Flag: Disallowed