Loss of BMPER induces leukocyte adhesion and extravasation. (A) Loss of BMPER increases dynamic adhesion of PBMCs on the endothelial surface in flow chamber experiments. Endothelial cells were transfected with siBMPERII or scrambled siRNA. TNFα-stimulated endothelial cells served as a positive control. PMA (phorbol-12 myristate-13acetate) activated PBMCs attached on the endothelial surface (left panel: representative images; top: phase contrast, bottom fluorescence). (B) Intravital microscopy of mesenterial veins revealed more leukocyte adhesion in BMPER± mice (n = 6) compared with control (n = 5). Mice were treated with TNFα (10ng/g bw IP) 4 hours before intravital microscopy. Leukocytes and thrombocytes were labeled with Rhodamin 6G (*P < .05). (C) At baseline levels, there was no difference in peripheral white blood cell (WBC) counts between BMPER± and wild-type control mice. (D) Leukocyte extravasation is increased in thioglycollate-induced peritonitis in BMPER ±mice. At 4 hours after challenge with 2 mL of 4% thioglycollate IP BMPER ±mice (n = 5) showed more extravasation of leukocytes to inflamed peritoneum compared with control mice (n = 5). Leukocytes were collected by peritoneal lavage and total leukocyte count was analyzed by hemocytometer (*P < .05 versus WT control).