gms | German Medical Science

28. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

24. bis 27.11.2004, Hannover

Increased activation of NFAT by the Angiotensin-(1-7)/Mas signaling pathway

Erhöhte Aktivierung von NFAT in der Angiotensin(1-7)/Mas Signalkaskade

Meeting Abstract (Hypertonie 2004)

Search Medline for

  • J. Zhang - Charité Berlin-Campus Benjamin-Franklin (Berlin, D)
  • F. Gembardt - Charité Berlin-Campus Benjamin-Franklin (Berlin, D)
  • Y. Wang - Erasmus Medical Center (Rotterdam, NL)
  • 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. Doc04hochP45

The electronic version of this article is the complete one and can be found online at:

Published: August 10, 2005

© 2005 Zhang et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.



Angiotensin-(1-7) was recently found to be an endogenous ligand for the G protein-coupled receptor Mas. Unclear factors of activiated T cells (NFAT) is a ubiquous transcription factor which plays an important role in cardiovascular and skeletal muscle development. The aim of our study is to investigate the signaling pathway between Ang-(1-7)/Mas axis and NFAT. HEK293 cells were transiently transfected by pcDNA3.1RNMas and pNFAT-TA -Luc alone or in combination and the transfected cells were maintained in serum-free DMEM (Dulbecco's Modified Eagle Medium). The luciferase product was measured 24h after transfection. In Mas-transfected cells, the lucifersase activity (fold to control) dose-dependently increased with an increasing amount of Mas (5-100ng), and A-779 (10-6M), a specific antagonist of Ang-(1-7), had no blocking effect on the increased activation of NFAT induced by Mas. In none-Mas transfected cells, the luciferase activity was increased with the increase of Ang-(1-7) (10-11 to 10-5M), and A-779 (10-6M), Irbersatan (an antagonist of Ang II receptor type 1, AT1, 10-6M), PD123319 (an antagonist of Ang II receptor type 2, AT2, 10-6M),and HOE140 (an antagonist of Bradykinin B2 recepotor type 2, B2, 10-6M) could not block the increased activation of NFAT induced by Ang-(1-7). The data showed that Mas constitutively activiate NFAT, and Ang-(1-7) could increase the activation of NFAT via a Mas, AT1, AT2 and B2 independent receptor.