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 1
Correlation of CVB3-induced cardiac injury and JAK-STAT activation. (a) Mice were infected with CVB3. Protein lysate from the heart was blotted at the indicated days after CVB3 inoculation and probed with the antibodies indicated. (b) Northern blot of total RNA from the heart after CVB3 inoculation was probed for IRF1, FcγRI, SOCS1, and SOCS3 expression. 28S and 18S RNA are shown as controls. (c) Virus titer and the disruption of cardiac cell membrane within 5 days after CVB3 inoculation. Four-week-old male Balb/c mice were inoculated with 10³ PFUs of CVB3 intraperitoneally and sacrificed at the day indicated. Evans blue dye was injected intraperitoneally 4 hours before the sacrifice (4). The left panel shows the time course of virus titer (solid line) and the percentage of Evans blue dye–positive area in the heart (gray bars). The Evans blue dye–positive areas were quantitated using NIH image software (NIH, Bethesda, Maryland, USA). The right panels show Evans blue dye–negative (Day 0) and positive (Day 3) sections (the brighter red staining areas). The data were collected from three mice for each time point and expressed as means ± SE. (d) Dual immunostaining of the infected heart demonstrates that the cells that are positive for Evans blue dye are also positive for viral capsid proteins. The left panel shows immunofluorescent staining with anti-CVB3 antibody (green), and the center panel shows Evans blue dye (red) uptake in the same field. The right panel is a merged image. Scale bars: 1 mm (c); 50 μm (d). P-STAT1, phospho-STAT1; P-STAT3, phospho-STAT3.