Mimicking phosphorylation at Ser-48 strongly reduces surface expression of human macrophage scavenger receptor class A: implications on cell motility.

The role of human macrophage scavenger receptor A1 (SRA1) in the development of atherosclerotic lesions is still scarcely defined. Substituting serine 48 in human SRA1 by an aspartate demonstrated that (1) surface expression of the mutated receptor was 13-fold decreased; (2) the amount of cell-associated Texas red-labeled acetylated low density lipoprotein (LDL) in mutant receptor-expressing cells was almost three-fold reduced; (3) the migration of mutant receptor-transfected cells towards surfaces coated with oxidized LDL decreased by almost 60% compared to cells that were transfected with the wild type receptor. Phosphorylation of the cytoplasmic part of SRA1 may help to modulate the residence time of macrophages in atherosclerotic lesions.