Fig. 7

Up-regulated VCAM-1 by TNF-α contributes to enhancement of monocyte adhering to HCFs. a For adhesion activity, cells were pretreated with Act. D (transcription inhibitor, 10 μM), CHI (translation inhibitor, 1 μM), TNFR-nAb (10 μg/ml), PP1 (c-Src, inhibitor, 1 μM), AG1478 (EGFR inhibitor, 10 μM), LY294002 (PI3K inhibitor, 10 μM), SH-5 (Akt inhibitor, 1 μM), or Bay11-7082 (NF-κB inhibitor, 3 μM) for 1 h and then incubated with TNF-α (15 ng/ml) for 16 h prior to the addition of THP-1 monocytes. The adhesion activity was determined by cell adhesion assay as described in Fig. 1. Data are expressed as mean ± SEM of at least three individual experiments (n = 3). ^# P < 0.01 vs. TNF-α alone. b Schematic presentation of the summary of this work. In HCFs, TNF-α/TNFR1-mediated signaling pathways linked to up-regulation of VCAM-1. TNF-α induces VCAM-1 expression via c-Src-dependent transactivation of EGFR/PI3K/Akt cascade linking to p65 NF-κB transcription activity. Finally, TNF-α-up-regulated VCAM-1 contributes to enhancement of monocyte adhering to HCFs