Fig. 5: Effect of APC on cell adhesion molecule expression and leukocyte–endothelial cell adhesion.
From: Elucidating mechanisms of genetic cross-disease associations at the PROCR vascular disease locus
a Barplots showing gene expression levels of ICAM1 and PROCR in human umbilical vein endothelial cells (HUVECs) and human coronary artery endothelial cells (HCAECs) relative to the control condition (i.e., 0 nM APC; indicated with a dashed line). Cells were co-incubated with 1 ng/ml TNF-α and varying concentrations of APC (0, 0.1, 1, 10, 100 nM) for 24 h. Data are shown for n = 5 (ICAM1) and n = 4 (PROCR) biological replicates in HUVECs and n = 4 (ICAM1) and n = 5 (PROCR) biological replicates in HCAECs. Error bars show standard deviations of the means. The blue and green lines indicate the fitted linear regression model for gene expression level~log(APC concentration). P values for the F-test of the linear regression model are shown. For each biological replicate, three technical replicates were averaged. b Barplots showing mean cell adhesion events using static adhesion assays with PMA-stimulated monocytic cells (U937) and TNF-α-activated HUVECs or HCAECs. Cells were co-incubated with 1 ng/ml TNF-α and 100 nM APC for 24 h (Methods). Data are shown for n = 5 and n = 4 biological replicates in HUVECs and HCAECs, respectively. Error bars show standard deviations of the means. P values were calculated using paired one-tailed t-tests. For each biological replicate, 2–4 technical replicates were averaged.
