Increased atherosclerotic lesion regression following blockade of JAM-C is concurrent with increased leukocyte emigration from plaques.

<p>48-hrs prior to transplantation or immediate sacrifice, all donor ApoE^-/- mice fed 12-wks of WD were injected with EdU (2mg/kg, i.p) to incorporate into DNA of monocyte precursors proliferating in the bone marrow. EdU-labeled circulating monocytes then enter the circulation and are recruited into atherosclerotic plaques. (A) Emigration from the plaques was quantified as the decrease in the number of EdU⁺ cells per section in the aortic arch plaques in baseline mice, compared to after transfer to the normolipidemic recipients. (B) Donor mice sacrificed at the transplant time point show robust EdU⁺ labeling in the aortic arch lesions. Recipient mice sacrificed 4-days after transplantation show significant reduction of EdU⁺ cells, indicating emigration during regression. (C) Recipient mice in which JAM-C was blocked via injections (JAM-C antibody) demonstrate even higher leukocyte egress than recipients treated with the isotype control (not shown) or (D) PBS buffer control. Lesions are outlined from endothelium with dashed white line. Data are presented as the mean value ±SEM (N = 6). ** = P<0.01 compared to baseline measurements. § = P<0.05 compared to WT and IgG recipients.