6533b862fe1ef96bd12c7645

RESEARCH PRODUCT

Cholesterol accumulation is increased in macrophages of phospholipid transfer protein-deficient mice: normalization by dietary alpha-tocopherol supplementation.

Valérie DeckertAlexis KleinGinette BessèdeCatherine DesrumauxAnne AthiasNaig Le GuernNicolas OgierLaurent Lagrost

subject

medicine.medical_specialtymedicine.medical_treatmentalpha-TocopherolOxidative phosphorylationBiologychemistry.chemical_compoundMiceIn vivoPhospholipid transfer proteinInternal medicineMalondialdehydeExtracellularmedicineAnimalsTocopherolPhospholipid Transfer ProteinsMice KnockoutCholesterolVitamin EVitaminsLipoproteins LDLEndocrinologyCholesterolchemistryBiochemistryDietary SupplementsMacrophages Peritoneallipids (amino acids peptides and proteins)Cardiology and Cardiovascular Medicinealpha-Tocopherol

description

Objective— Phospholipid transfer protein (PLTP) is a multifunctional, extracellular lipid transport protein that plays a major role in lipoprotein metabolism and atherosclerosis. Recent in vivo studies suggested that unlike systemic PLTP, macrophage-derived PLTP would be antiatherogenic. The present study aimed at characterizing the atheroprotective properties of macrophage-derived PLTP. Methods and Results— Peritoneal macrophages were isolated from PLTP-deficient and wild-type mice and their biochemical characteristics were compared. It is shown that macrophages isolated from PLTP-deficient mice have increased basal cholesterol content and accumulate more cholesterol in the presence of LDL compared with wild-type cells. Cholesterol parameters in macrophages of PLTP-deficient mice were normalized by dietary α-tocopherol supplementation. Conclusions— The antiatherogenic properties of macrophage-derived PLTP are related at least in part to its ability to reduce cholesterol accumulation in macrophages through changes in the α-tocopherol content and oxidative status of the cells.

10.1161/atvbaha.107.151753https://pubmed.ncbi.nlm.nih.gov/17717294