Gain-of-function mutant of angiotensin II receptor, type 1A, causes hypertension and cardiovascular fibrosis in mice
J. Clin. Invest. Sandrine Billet, et al. 117:1914 doi:10.1172/JCI28764 [Go to this article.]

Figure 3
Signaling properties of AT_1A in tissues and primary hepatocyte cultures from AT_1AWT and AT_1AMUT mice. (A) Basal phosphorylation of STAT1, STAT3, and ERK1/2 in the liver. Left: Representative Western blot for 3 AT_1AWT and 3 AT_1AMUT mice. Right: Histograms show mean ± SEM of the ratio of phosphorylated protein to total protein and expressed as a percentage of this ratio in AT_1AWT corresponding tissue. White bars, AT_1AWT; black bars, AT_1AMUT. *P < 0.05 compared with AT_1AWT. (B and C) Stimulation of ERK1/2 phosphorylation by Ang II (B) and Ang IV (C). Primary cultured hepatocytes from AT_1AWT (black squares) and AT_1AMUT (white triangles) mice were serum-starved for 3 hours and stimulated with Ang II (B) or Ang IV (C) for 5 minutes at 37°C. Left panels show representative immunoblots of phosphorylated ERK1/2 (p-ERK1/2) and total ERK1/2 (ERK1/2). ERK1/2 phosphorylation was quantified by densitometry, normalized to the amount of total ERK1/2 in each lane and expressed as a percentage over basal phosphorylation of ERK1/2 as shown in the right panels. Results are mean ± SEM of 3 independent experiments.