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Fig. 1 | The Journal of Physiological Sciences

Fig. 1

From: Epac activation inhibits IL-6-induced cardiac myocyte dysfunction

Fig. 1

Effects of various cytokines on signal transducer and activator of transcription (STAT) phosphorylation and the time course of interleukin (IL)-6-mediated STAT phosphorylation. a Phosphorylation of signal transducer and activator of transcription 3 (STAT3) at Tyrosine 705 (Tyr705) was examined at 30 min after treatment with IL-6 (30 ng/ml), IL-1β (10 ng/ml), IL-10 (10 ng/ml), IL-17 (10 ng/ml), interferon gamma (IFN-γ; 10 ng/ml), keratinocyte-derived chemokine (KC; 50 ng/ml), monocyte chemotactic protein-1 (MCP-1; 10 ng/ml), RANTES (regulated upon activation, normal T cell expressed and secreted; 10 ng/ml), and tumor necrosis factor alpha (TNF-α; 10 ng/ml). The phosphorylation was upregulated by 14-fold in response to IL-6 (n = 4, *significantly different at p < 0.05, Student’s t test). T-STAT Total STAT, P-STAT phosphorylated STAT. b Phosphorylation of signal transducer and activator of transcription 1 (STAT1) at Tyrosine 701 (Tyr701) was examined at 30 min after treatment with IL-6 (30 ng/ml), IL-1β (10 ng/ml), IL-10 (10 ng/ml), IL-17 (10 ng/ml), IFN-γ (10 ng/ml), KC (50 ng/ml), MCP-1 (10 ng/ml), RANTES (10 ng/ml) and TNF-α (10 ng/ml). The phosphorylation was upregulated by 13-fold in response to IFN-γ and by 2-fold in response to IL-6 (n = 4, *significantly different at p < 0.05, Student’s t test). c Time course of IL-6 (30 ng/ml)-mediated STAT3 phosphorylation at Tyr705. Phosphorylation peaked at 30 min after treatment with IL-6 (30 ng/ml) and then decreased gradually [n = 4, ****significantly different at p < 0.0001 vs. 0 h, one-way analysis of variance (ANOVA)]. d Time course of IL-6 (30 ng/ml)-mediated phosphorylation of STAT1 at Tyr701. Phosphorylation peaked at 30 min after treatment with IL-6 and then decreased gradually (n = 4–6, ****significantly different at p < 0.0001 vs. 0 h, one-way ANOVA). Data are presented as the mean ± standard error of the mean (SEM)

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