Apolipoprotein J inhibits the migration and adhesion of endothelial cells

Background. Apolipoprotein J (ApoJ) is expressed after vascular injury and remodeling and may inhibit endothelial cell activation in the vascular wall . Recently, ApoJ was identified as upregulated in hyperplastic lesions afte r prosthetic arterial grafting. This study analyzed the effect of ApoJ on h uman umbilical vein endothelial cell (HUVEC) migration, adhesion, and proli feration. Methods. Cell migration towards ApoJ + fetal bovine serum (FBS) or vascular endothelial growth factor (VEGF) was evaluated with the use of a microchem otaxis chamber with or without a fibronectin-coated membrane. For migration that involved fibronectin, cells were exposed to ApoJ before or after plac ement on the membrane. Cell adhesion to fibronectin was studied similarly b ut without stimulant. The vital dye alamar blue assessed proliferation of A poJ + FBS- or VEGF-stimulated HUVECs. Results. ApoJ alone did not cause migration or proliferation of HUVECs. Wit hout fibronectin, ApoJ decreased the migration of HUVECs towards FBS or VEG F When fibronectin was introduced, ApoJ decreased cell migration toward FBS or VEGF and decreased adhesion only when HUVECs in solution were exposed t o ApoJ before the placement oil fibronectin. ApoJ had no effect on FBS- or VEGF-induced proliferation. Conclusions. ApoJ inhibits HUVEC migration and adhesion. By altering endoth elial function during vascular injury, ApoJ appears to regulate, in part, t he early development of intimal hyperplasia after prosthetic arterial graft ing.