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Fig. 5 | Journal of Biomedical Science

Fig. 5

From: Tumor necrosis factor-alpha induces VCAM-1-mediated inflammation via c-Src-dependent transactivation of EGF receptors in human cardiac fibroblasts

Fig. 5

TNF-α induces VCAM-1 expression via PI3K/Akt cascade. a, b Cells were pretreated with various concentrations of LY294002 (PI3K inhibitor; 0.1, 1, or 10 μM) or SH-5 (Akt inhibitor; 0.01, 0.1, or 1 μM) for 1 h and then incubated with TNF-α for 16 h (a) or 4 h (b). c Time dependence of TNF-α-induced Akt phosphorylation, cells were treated with TNF-α (15 ng/ml) for the indicated time intervals in the presence or absence of LY294002 (10 μM). d Cells were transfected with siRNA of p110 (a PI3K subunit), Akt, or scramble (scrb, as a control) for 24 h and then incubated with TNF-α for 16 h. e Cells were treated with TNF-α for the indicated time intervals in the presence or absence of TNFR nAb (10 μg/ml), c-Src siRNA, or AG1478 (10 μM). The VCAM-1 protein (a, d), and mRNA and promoter activity (b) were analyzed by Western blotting, real time-PCR, and promoter assay, respectively. The Akt phosphorylation (c, e) was analyzed by Western blot. Data are expressed as mean ± SEM of three individual experiments (n = 3). * P < 0.05, # P < 0.01 vs. TNF-α alone

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