The suppressor of cytokine signaling–1 (SOCS1) is a novel therapeutic target for enterovirus-induced cardiac injury
J. Clin. Invest. Hideo Yasukawa, et al. 111:469 doi:10.1172/JCI16491 [Go to this article.]

Figure 2
Increased myocardial injury, virus replication, and mortality in SOCS1 transgenic mice. (a) Expression of Myc-tagged SOCS1 in the heart was compared among four SOCS1 transgenic lines (A–D) by immunoblotting with anti-Myc antibody (upper panel). Heart tissue extracts for protein (lower left panel) and RNA (lower right panel) from two lines of wild-type and two lines of transgenic mice (A and B) were prepared three days after CVB3 inoculation and probed as shown. (b) Wild-type and SOCS1 transgenic mice (4-week-old males) were inoculated with 10³ PFUs of virus (n = 15). The survival rate in infected, SOCS1 transgenic mice was significantly lower than in infected, wild-type littermates (P < 0.0001). (c) Evans blue dye uptake in the heart was markedly increased in surviving SOCS1 transgenic mice on day 4 after infection (red stain, left panels). The percent area of Evans blue staining in the hearts is shown (right panel; mean ± SE, n = 3, *P < 0.01). (d) Increased viral titer in the heart but not the liver of SOCS1 transgenic mice. Virus titers in SOCS1 transgenic and wild-type hearts and livers from 3–5 days after infection (mean ± SE, n = 3, *P < 0.01 comparing SOCS1 transgenic mice with wild-type littermates). (e) Hematoxylin and eosin stains of representative wild-type and SOCS1 transgenic mouse hearts 4 days after infection. Note the thrombus in the center of the ventricle (right panel). Scale bars: 1 mm (c); 100 μm (e, middle); 200 μm (e, right). Tg, transgenic; P-STAT1, phospho-STAT1; P-STAT3, phospho-STAT3.