gms | German Medical Science

28. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

24. bis 27.11.2004, Hannover

Pattern of angiotensin II-stimulated transcription factors is cell-type specific

Das Muster der Angiotensin II stimulierten Transkriptionsfaktoren ist Zelltyp spezifisch

Meeting Abstract (Hypertonie 2004)

Suche in Medline nach

  • presenting/speaker R. Ziegleder - Erasmus Medical Center (Rotterdam, NL)
  • presenting/speaker A. Heiss - Charité Berlin - Campus Benjamin Franklin (Berlin, D)
  • presenting/speaker J. Zhang - Charité Berlin - Campus Benjamin Franklin (Berlin, D)
  • presenting/speaker T. Walther - Erasmus Medical Center (Rotterdam, NL)

Hypertonie 2004. 28. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Hannover, 24.-27.11.2004. Düsseldorf, Köln: German Medical Science; 2005. Doc04hochP46

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter:

Veröffentlicht: 10. August 2005

© 2005 Ziegleder et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen ( Er darf vervielf&aauml;ltigt, verbreitet und &oauml;ffentlich zug&aauml;nglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.



Angiotensin (Ang) II, the major biologically active peptide of the renin-angiotensin system (RAS), exerts numerous actions on the cardiovascular system via the Ang II AT1 receptor, such as vasoconstriction and electrolyte balance, by mediating cell-type-specific calcium release and activation of a variety of transcription factors. Therefore we investigated the capability of Ang II to stimulate the transcription factors nuclear factor-kappaB (NFKB), nuclear factor of activated T-cells (NFAT) and activator protein-1 (AP1) via AT1 activation in two different cell lines, to determine cell-type-specific differences in the intracellular signaling mediated by the AT1 receptor.

HEK293 and COS-1 cells, transfected with a plasmid containing the AT1 cDNA, driven by a CMV promoter, were used for dual luciferase assays. For measurements the cells were co-transfected with plasmids encoding for firefly-luciferase driven by an NFKB-, NFAT-, or AP1-induced promoter and a plasmid encoding renilla-luciferase, which was used as an internal control. Cells were stimulated with Ang II (10-6 M) and the luciferase activity was measured 8 hours after the stimulation.

In both cell lines, increasing concentrations of the AT1 receptor led to a dose-dependent increase in luciferase production, whereas in HEK293 cells the luciferase activity was increased 5.2 fold by NFKB (baseline: unstimulated, AT1-untransfected HEK293 cells), 9.1 fold by NFAT and 23.8 fold by AP1. In COS-1 cells the luciferase activity was increased 1.8 fold by NFKB (baseline: unstimulated, AT1-untransfected COS-1 cells), 3.7 fold by NFAT and 3.1 fold by AP1.

Our results demonstrate the pattern of angiotensin II stimulated transcription factors is cell-type specific. This finding could be of great clinical relevance, since pharmacological targeting the AT1 receptor downstream could lead to cell-type-specific beneficial treatment properties.