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. 2014 Jan;184(1):200–213. doi: 10.1016/j.ajpath.2013.09.010

Figure 7.

Figure 7

Role of PKCδ in PMVEC adhesion molecule expression. The expression of VCAM-1, ICAM-1, and PECAM-1 on PMVEC monolayers was determined by a cell-surface ELISA. Human PMVEC monolayers were treated overnight with buffer or IL-1β ± PKCδ inhibitor (0.01 to 5 mol/L). A: IL-1β–stimulated VCAM-1 expression. Constitutive expression of VCAM-1 (buffer) was normalized to 1, and expression in response to IL-1β treatment ± PKCδ inhibitor was compared with constitutive VCAM-1 expression. B: IL-1β–stimulated ICAM-1 expression, relative to constitutive ICAM-1 expression (as described for A). C: IL-1β–stimulated PECAM-1 expression, relative to constitutive PECAM-1 expression (as described for A). Data are expressed as means ± SEM. n = 7 (A); n = 5 (B); n = 6 (C). ∗∗P < 0.01, buffer versus IL-1β–treated PMVECs, †P < 0.01, IL-1β–treated PMVECs versus 10 U/mL IL-1β+PKCδ inhibitor (0.1–5 μmol/L) (A). ∗P < 0.05, IL-1β–treated PMVECs versus IL-1β+PKCδ inhibitor (0.1 μmol/L); ∗∗P < 0.01, IL-1β–treated PMVECs versus IL-1β+PKCδ inhibitor (1–5 μmol/L); and ∗∗∗P < 0.001, buffer versus IL-1β–treated PMVECs (B).