In this study, we tested the role of leukocyte PDZK1 in atherosclerosis development by using bone marrow transplantation to generate ldlr deficient mice lacking PDZK1 in leukocytes.
Identification of carriers of rare mutations in human SCARB1 and PDZK1 that impair the function of their gene products and characterization of the effects of these mutations on HDL cholesterol levels and atherosclerosis will add to our understanding of the importance of HDL function and cholesterol flux, as opposed to HDL-cholesterol levels, per se, for protection against cardiovascular disease.
PDZK1 plays an essential role in maintaining hepatic SR-BI levels and controlling HDL metabolism, protects against the development of atherosclerosis in a murine model and also mediates SR-BI-dependent regulation of endothelial cell biology by HDL, suggesting that PDZK1 plays multiple roles in normal physiology and may influence associated disorder.