Apolipoprotein A-I and lecithin:cholesterol acyltransferase transfer induce cholesterol unloading in complex atherosclerotic lesions

Lecithin:cholesterol acyltransferase: old friend or foe in atherosclerosis?

“…However, the intima/media ratio tended to be lower compared with the animals treated with an empty adenovirus, indicating that LCAT overexpression slowed the progression of atherosclerosis. Interestingly, adenoviral LCAT overexpression also induced cholesterol unloading of the lesions, consistent with enhanced RCT from the arterial wall ( 140 ). Zhen et al recently applied the adeno-associated viral vector serotype 8 (AAV8) for liver-directed delivery of human LCAT in heterozygous LDL receptor knockout mice expressing CETP ( 141 ).…”

“…heterozygous LDL receptor knockout rabbits (62.5% New Zealand White and 37.5% Japanese White) a 0.15% cholesterol diet for 420 days ( 140 ). Adenoviral LCAT overexpression increased HDL cholesterol 1.9-fold, whereas non-HDL cholesterol was not affected.…”

Protective molecules and their cognate antibodies: new players in autoimmunity

“…Therefore, it is clear that a deficiency of Apo A-1 and HDL is an important risk factor for atherosclerosis [16,69].…”

The relative atherogenicity of VLDL and LDL is dependent on the topographic site

“…Lipoprotein ultracentrifugation and plasma lipid analysis were performed as described previously ( 21 ). Phospholipids were quantifi ed by the Wako Phospholipids B assay (Wako Chemical GMBH, Neuss, Germany) according to the instructions of the manufacturer.…”

“…All experiments were conducted in conformity with the Public Health Service Policy on Humane Care and Use of Laboratory Animals and were approved by the Institutional Animal Care and Research Advisory Committee of the University of Leuven. Blood sampling and determination of the LDLr genotype were performed as described before ( 21,22 ).…”