Ectopic beta-chain of ATP synthase is an apolipoprotein A-I receptor in hepatic HDL endocytosis.

摘要: The effect of high-density lipoprotein (HDL) in protecting against atherosclerosis is usually attributed to its role 'reverse cholesterol transport'. In this process, HDL particles mediate the efflux and transport from peripheral cells liver for further metabolism bile excretion. Thus, cell-surface receptors on hepatocytes are chief partners regulation homeostasis. A high-affinity receptor apolipoprotein A-I (apoA-I) was previously identified surface hepatocytes. Here we show that identical beta-chain ATP synthase, a principal protein complex mitochondrial inner membrane. Different experimental approaches confirm ectopic localization components synthase presence hydrolase activity at hepatocyte cell surface. Receptor stimulation by apoA-I triggers endocytosis holo-HDL (protein plus lipid) mechanism depends strictly generation ADP. We perfused rat ex vivo using specific inhibitor synthase. membrane-bound has unsuspected modulating concentrations extracellular ADP regulated plasma apolipoprotein.