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. 2017 Jun 1;7(8):2186–2203. doi: 10.7150/thno.18407

Figure 1.

Figure 1

IL-32α inhibits endothelial inflammation in vitro. (A,B) Immortalized mouse arterial endothelial cells (iMAECs) were cultured in 24-well culture plates for 24 h, then transfected with human IL-32α-expressing pcDNA3.1+-6 × Myc vector (hIL-32α-vector) or control vector. After 24 h, cells were treated with recombinant tumor necrosis factor α protein (TNFα) (10 ng/mL; 24 h), and (A) VCAM-1 and ICAM-1 mRNA expression was determined by qPCR (data shown as mean ± SEM; n = 5, *p < 0.05 by Student's t-test) and (B) Myc-tag, IL-32α, VCAM-1, and ICAM-1 proteins were analyzed by western blotting. (C) iMAECs were treated with recombinant human IL-32α protein (rhIL-32α) for 24 h, and then treated with TNFα for 24 h. Cells were lysed and analyzed by western blotting with antibodies against VCAM-1 and ICAM-1, using β-actin as a loading control. For monocyte adhesion assays, iMAECs and human umbilical vein endothelial cells (HUVECs) were (D) transfected with hIL-32α-vector or (E) treated with rhIL-32α for 24 h, then treated with TNFα (10 ng/mL; 24 h), and THP-1 monocyte adhesion to endothelial cells was determined (data shown as mean ± SEM; n = 6, *p < 0.05 by Student's t-test).