gms | German Medical Science

29. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

Deutsche Hochdruckliga e. V. DHL ® - Deutsche Hypertonie Gesellschaft Deutsches Kompetenzzentrum Bluthochdruck

23. bis 25.11.2005, Berlin

Divergent roles of angiotensin AT1 and AT2 receptors in myocardial ischemia-induced apoptosis and inflammation

Meeting Abstract

Suche in Medline nach

  • J. Li - Charité - Universitätsmedizin Berlin, Center for Cardiovascular Research (CCR) (Berlin, D)
  • K. Elkhrbash - Charité - Universitätsmedizin Berlin, Center for Cardiovascular Research (CCR) (Berlin, D)
  • M. Timm - Charité - Universitätsmedizin Berlin, Center for Cardiovascular Research (CCR) (Berlin, D)
  • T. Unger - Charité - Universitätsmedizin Berlin, Center for Cardiovascular Research (CCR) (Berlin, D)

Hypertonie 2005. 29. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Berlin, 23.-25.11.2005. Düsseldorf, Köln: German Medical Science; 2006. Doc05hochP87

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/hoch2005/05hoch087.shtml

Veröffentlicht: 8. August 2006

© 2006 Li et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielf&aauml;ltigt, verbreitet und &oauml;ffentlich zug&aauml;nglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Previous studies have revealed that cardiac angiotensin AT1 and AT2 receptors are upregulated in response to acute myocardial infarction (MI). However, the cell sources of these angiotensin receptors and their potential relevance in cardiac apoptosis and inflammation are not yet defined. We characterized cardiac apoptosis and inflammation by evaluating cardiac expression of proapoptotic proteins (p53, Bax, caspase-3) and cytokines (IL-2, IL-1beta, IL-10), respectively, seven days after MI in rats. Western Blot analysis showed that cardiac p53, Bax, caspase-3 as well as IL-1beta and IL-10 were significantly upregulated. Immunofluorescence labeling further demonstrated that both AT1 receptor and p53 were colocalized in cardiomyocytes in the border-zone of the infarction whereas AT2 receptor and IL-10 were co-expressed in ED1+ macrophages in the peri-infarct region. Blocking AT1 receptors by valsartan dramatically suppressed the expression of p53, Bax and caspase-3 but enhanced the expression of IL-10, whereas blocking AT2 receptors by PD 123319 failed to influence theses proapoptotic proteins, but significantly attenuated IL-10 expression. These results suggest the divergent roles of AT1 and AT2 receptors in cardiac apoptosis and inflammation. AT1 receptors may initiate cardiomyocyte apoptosis by inducing p53-triggered apoptotic cascade whereas AT2 receptors may exert an anti-inflammatory effect by mediating cardiac IL-10 expression in myocardial infiltrating macrophages.