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 5
Augmentation of the JAK/STAT pathway by dnSOCS1 in cardiac myocytes. (a and b) Cardiomyocytes were transfected with a plasmid mixture containing the APRE-luciferase reporter gene (200 ng), the NF-κB–luciferase reporter gene (200 ng), the β-galactosidase gene (100 ng), the AAV shuttle plasmid, or the indicated concentrations of dnSOCS1 plasmid. After transfection, cells were incubated in the presence or absence of 1 nM CT-1 or 20 ng/ml TNF-α for 6 hours, and cell extracts were prepared. Data normalized with the β-galactosidase activity are shown. The experiments were repeated three times. Results are expressed as means ± SD. *P < 0.01 for the comparison of CT-1 with the AAV shuttle. **P < 0.01 for the comparison of CT-1 with pcDNA3-SOCS1. (c) Time course of IFN-γ–induced STAT1 activation and CT-1–induced STAT3 activation in cardiac myocytes. Myocytes were treated with adenovirus LacZ or adenovirus dnSOCS1, were serum depleted for 24 hours, and were then stimulated with 1000 ng/ml IFN-γ or 1 nM CT-1 for the indicated period, respectively. Total cell extracts were prepared and blotted with phospho-STAT1, STAT1, phospho-STAT3, and STAT3 antibodies. The dnSOCS1 expression was confirmed with an anti-Myc antibody. Data from one experiment are presented; two additional experiments yielded comparable results. P-STAT1, phospho-STAT1; P-STAT3, phospho-STAT3; APRE, acute-phase response element.