Skip to main content
. 2017 Dec 13;8:1766. doi: 10.3389/fimmu.2017.01766

Figure 3.

Figure 3

Cigarette smoke extract (CSE)-induced CXCL16 overexpression is decreased by RhoA, p38 mitogen-activated protein kinase (MAPK), and nuclear factor (NF)-κB inhibition in human umbilical arterial endothelial cells (HUAEC). (A) CXCL16 expression was determined by flow cytometey in endothelial cells preincubated or not with a RhoA inhibitor (C3 transferase, 2 µg/ml) for 4 h and then stimulated with 1% CSE for 24 h. Results are expressed as mean of fluorescence intensity (MFI) (n = 5 independent experiments). Values are expressed as mean ± SEM. *P < 0.05 relative to values in the medium group; +P < 0.05 relative to 1% CSE group. (B) HUAEC were transfected with RhoA siRNA or control siRNA. At 48 h post-transfection, cells were stimulated with 1% CSE for 24 h. CXCL16 expression was determined by flow cytometry. Results are expressed as MFI (n = 7 independent experiments). Values are expressed as mean ± SEM. **P < 0.01 relative to values in the medium group; +P < 0.05 relative to their respective group in control siRNA-transfected cells. (C) HUAEC were stimulated with 1% CSE for 24 h. Some cells were pretreated with PD098059 (20 µM), SB202130 (20 µM), or MOL-294 (2.5 µM) for 1 h before CSE stimulation. CXCL16 expression was determined by flow cytometry. Results are expressed as MFI (n = 4–7 independent experiments). Values are expressed as mean ± SEM. **P < 0.01 relative to values in the medium group; +P < 0.05 relative to values in the 1% CSE group.