IL-33 and ST2 comprise a critical biomechanically induced and cardioprotective signaling system
J. Clin. Invest. Shoji Sanada, et al. 117:1538 doi:10.1172/JCI30634 [Go to this article.]

Figure 5
IL-33/ST2 signaling is cardioprotective in vivo. (A) Echocardiographic analysis at 4 weeks after operation demonstrated increased left ventricular mass, left ventricular wall thickness, and reduced fractional shortening in ST2^–/– mice. Treatment with IL-33 reduced hypertrophy only in WT mice. IL-33 caused no significant change under non-stress conditions in vivo. n = 10 (nonoperated control); 8 (WT sham); 10 (WT TAC); 8 (WT sham + IL-33); 10 (WT TAC + IL-33); 8 (ST2^–/– sham); 12 (ST2^–/– TAC); 8 (ST2^–/– sham + IL-33); and 10 (ST2^–/– TAC + IL-33). (B) Representative images and (C) quantitative analysis of mRNA expression of ANP and BNP relative to internal control (18S) in the left ventricle at 1 week after operation, as assessed by Northern analysis. White and black bars indicate sham-operated and TAC, respectively. (D) NF-κB activation from EMSA in vivo 1 week after operation. ANP and BNP expression and NF-κB activity increased in ST2^–/– mice compared with WT mice; IL-33 reversed these changes only in WT mice. Positive and negative control mixtures as well as specific competition mixtures and supershift induce by p65 antibody are also shown. *P < 0.05 versus nonoperated control (A) or sham-operated WT (C); ^ΧP < 0.05 versus the same treatment in WT; ^†P < 0.05 versus sham in the same group; ^#P < 0.05.