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. 2016 Mar 18;6:23387. doi: 10.1038/srep23387

Figure 2. Rn inhibits the adhesion, cytokine release of the TLR2-stimulated THP-1 through blockade of integrin αVβ3.

Figure 2

(A) Adhesion and (B) TNFα production by Pam3CSK4-stimulated THP-1 cells seeded on plates coated with albumin (BSA), collagen (Col), fibrinogen (Fg), fibronectin (Fn) and vitronectin (Vn), in the absence (CTL) or presence of Rn (Rn, 30 μg/ml). (C) Pam3CSK4-activated THP-1 cells were incubated with increasing concentration of FITC-Rn before the fluorescence intensity measurement by flow cytometry. Total binding (square) and non-specific binding (circle) were determined by FITC-Rn and FITC-BSA, respectively. (D) Pam3CSK4-activated THP-1 cells were incubated with Rn (30 μg/ml, bold line) or not (thin line) before probing with anti-αVβ3 or anti-β2 mAbs, respectively. (E) THP1 cells were transfected with integrin αV (αV), integrin αM (αM) or negative control (NC) siRNA for 48 hr followed by different assays. Western blotting for integrin αV and TLR2 (left panel). TNFα release measured with the ELISA kit (right panel). Blank bar, untreated control (CTL). Black bar, incubated with Rn (Rn). Means ± SEM of three separate experiments were checked for statistical difference. *p < 0.05, **p < 0.01, ***p < 0.001, compared with Pam3CSK4-activated control groups (CTL).