Fig 1: ADK deficiency suppresses endothelial inflammation in vivo. a Representative images for immunohistochemical staining of VCAM-1 in aortas from TNF-α-treated ADKWT and ADKVEC-KO mice (scale bar, 50 µm). b Quantification of VCAM-1 expression in aortas from TNF-α-treated ADKWT and ADKVEC-KO mice and the graph shows the data as fold change compared with the vehicle-treated ADKWT mice (n = 4–5 mice per group). c Representative images for immunohistochemical staining of ICAM-1 in aortas from TNF-α-treated ADKWT and ADKVEC-KO mice (scale bar, 50 µm). d Quantification of ICAM-1 expression in aortas from TNF-α-treated ADKWT and ADKVEC-KO mice and the graph shows the data as fold change compared with the vehicle-treated ADKWT mice (n = 4–5 mice per group). e RT-PCR analysis of mRNA levels of adhesion molecules in aortas from TNF-α-treated ADKWT and ADKVEC-KO mice (n = 5 mice per group). f Representative images of leukocyte rolling and adhesion on the endothelium of postcapillary venules in the cremaster muscles of vehicle or TNF-α-treated ADKWT and ADKVEC-KO mice. Rolling and adherent cells are indicated with dotted and solid circle line, respectively (scale bar, 20 µm). g Rolling velocity of leukocytes (at least 60 rolling leukocytes in 12 postcapillary venules of four mice per group). h Rolling number of leukocytes (at least 24 postcapillary venule segments in four mice per group). i Number of adherent leukocytes (at least 24 postcapillary venule segments in four mice per group). For bar graphs, data are the mean ± SEM, *P < 0.05 and **P < 0.01 (unpaired, two-tailed Student’s t-test)