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

Angiotensin II suppresses TNFa-induced IL-6 mRNA expression via the AT2-receptor in human dermal fibroblasts

Angiotensin II suppresses TNFa-induced IL-Angiotensin II über den AT2-Rezeptor verringert die durch TNFalpha induzierte Expression von Il-6 in humanen, dermalen Fibroblasten

Meeting Abstract

  • U. Steckelings - Charité - Universitätsmedizin Berlin, Center for Cardiovascular Research, Berlin (Berlin, D)
  • F. Rompe - Charité - Universitätsmedizin Berlin, Center for Cardiovascular Research, Berlin (Berlin, D)
  • J. Reinemund - Charité - Universitätsmedizin Berlin, Center for Cardiovascular Research, Berlin (Berlin, D)
  • M. Artuc - Charité - Universitätsmedizin Berlin, Center for Cardiovascular Research, Berlin (Berlin, D)
  • T. Unger - Charité - Universitätsmedizin Berlin, Center for Cardiovascular Research, Berlin (Berlin, D)

Hypertonie 2005. 29. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Berlin, 23.-25.11.2005. Düsseldorf, Köln: German Medical Science; 2006. Doc05hochP134

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/hoch2005/05hoch134.shtml

Veröffentlicht: 8. August 2006

© 2006 Steckelings 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

Recently, we demonstrated the presence of a complete renin-angiotensin-system in human skin. However, the characterisation of cutaneous actions of angiotensin II (Ang II) is only at the very beginning. Aiming to test whether Ang II may be involved in cutaneous inflammation, we examined IL-6 expression in response to Ang II with or without co-stimulation by TNFalpha and distinguished between AT1- and AT2-receptor mediated responses. Human primary dermal fibroblasts (passage 3 to 5) were isolated from female thoracic skin derived in the course of cosmetic breast surgery. Fibroblasts were stimulated with Ang II (10-7 M) for 24 hours and co-incubated with irbesartan (10-5 M; AT1-receptor antagonist) or PD 123319 (10-5 M; AT2-receptor antagonist), respectively. The same experiment was performed on a second set of cells, additionally treated with TNFalpha (10 ng/ml) in order to stimulate Il-6 expression and to examine the effect of Ang II on elevated Il-6 levels. Il-6 mRNA was detected by Real-Time-PCR.Ang II stimulated Il-6 expression fivefold. This stimulation could be inhibited by irbesartan, but not by PD 123319. TNFalpha caused a marked increase in Il-6 expression, which could be inhibited by AT2-receptor stimulation (Ang II in the presence of irbesartan). Thus, in human dermal fibroblasts, Il-6 expression is stimulated by TNFalpha and to a lesser extent by Ang II via the AT1-receptor. In contrast, Ang II via the AT2-receptor diminishes TNFalpha induced Il-6 expression. Consequently, Ang II may be involved in cutaneous inflammation by a dual mechanism: it acts pro-inflammatory via the AT1-receptor and anti-inflammatory via the AT2-receptor.