Cholesteryl Ester Transfer Protein and Atherogenesis

A single intravenous dose of endotoxin rapidly alters serum lipoproteins and lipid transfer proteins in normal volunteers

“…In the PLTP knock-out mouse, the catabolism of HDL, depleted of phospholipid, was markedly increased (47). CETP, which transfers cholesterol ester from HDL to VLDL and LDL, also decreased in mice transgenic for the human CETP gene and treated with endotoxin (51). The small, late changes in CETP in our human volunteers treated with endotoxin are consistent with the lack of change in HDL cholesterol.…”

Old and new findings on lipopolysaccharide-binding protein: a soluble pattern-recognition molecule

“…Both, human LBP and BPI are located in close proximity on chromosome 20 and share an intron-exon pattern with other human lipid-binding proteins, which was later also found to be characteristic of the entire BPI/LBP/PLUNC-like domain family [16][17][18][19]. Two human serum proteins, PLTP (phospholipid-transfer protein) and CETP (cholesteryl estertransfer protein), are important regulators of lipoprotein levels in humans and have received great attention as potential therapeutic targets in cardiovascular medicine [20,21]. Similarly to LBP (see below), within these proteins frequent mutations have also been described and linked to disease susceptibility [22,23].…”

Exploiting the Vascular Protective Effects of High-Density Lipoprotein and Its Apolipoproteins

“…35,36 Similarly, an elevated HDL level resulting from a deficiency of the cholesterol ester transfer protein (CETP) due to mutations in the CETP gene does not uniformly confer immunity against atherosclerosis. [37][38][39][40][41][42][43][44][45][46] In experimental animals, transgenic overexpression of lecithin cholesterol acyl transferase (LCAT) increases atherosclerosis, despite an in-crease in HDL, whereas hepatic overexpression of scavenger receptor (SR)-BI with gene transfer reduces atherosclerosis, despite a major reduction in HDL levels. 47,48 Furthermore, apolipoprotein A-I deficiency does not promote atherosclerosis in mice in the absence of elevated LDL or the overexpression of apolipoprotein B.…”