Apolipoprotein J inhibits the migration and adhesion of endothelial cells

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 after prosthetic arterial grafting. This study analyzed the effect of ApoJ on human umbilical vein endothelial cell (HUVEC) migration, adhesion, and proliferation.

Cell migration towards ApoJ + fetal bovine serum (FBS) or vascular endothelial growth factor (VEGF) was evaluated with the use of a microchemotaxis chamber with or without a fibronectin-coated membrane. For migration that involved fibronectin, cells were exposed to ApoJ before or after placement on the membrane. Cell adhesion to fibronectin was studied similarly but without stimulant. The vital dye alamar blue assessed proliferation of ApoJ + FBS- or VEGF-stimulated HUVECs.

ApoJ alone did not cause migration or proliferation of HUVECs. Without fibronectin, ApoJ decreased the migration of HUVECs towards FBS or VEGF. When fibronectin was introduced, ApoJ decreased cell migration toward FBS or VEGF and decreased adhesion only when HUVECs in solution were exposed to ApoJ before the placement on fibronectin. ApoJ had no effect on FBS- or VEGF-induced proliferation.

ApoJ inhibits HUVEC migration and adhesion. By altering endothelial function during vascular injury, ApoJ appears to regulate, in part, the early development of intimal hyperplasia after prosthetic arterial grafting.