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From the Department of Pediatrics (T.O., R.N., Y.I., I.M.), Kumamoto University School of Medicine, Kumamoto, the Department of Internal Medicine (K.S.), Fukuoka University, Fukuoka, and the Hiroshima Railway Hospital (K.T.), Hiroshima, Japan.
Correspondence to Dr Takao Ohta, Department of Pediatrics, Kumamoto University School of Medicine, 1-1-1 Honjo, Kumamoto-City Kumamoto 860, Japan. E-mail ohta@gpo.kumamotou.ac.jp.
Abstract We investigated the effects of subclasses of plasma LpA-I (HDL containing apoA-I but not apoA-II) on cholesterol esterification in plasma and net cholesterol efflux from foam cells. LpA-I was composed of particles of three diameters: large (11.1 nm; LgLpA-I), medium (8.8 nm; MdLpA-I), and small (7.7 nm; SmLpA-I). Plasma concentrations of LpA-I were positively correlated only with the level of LgLpA-I. Plasma concentrations of LgLpA-I were inversely correlated with the rate of cholesterol esterification in plasma and VLDL- and LDL-depleted plasma. Plasma concentrations of MdLpA-I and SmLpA-I did not correlate with the rate of cholesterol esterification in plasma or VLDL- and LDL-depleted plasma. When macrophage foam cells were incubated with Md and SmLpA-I, cellular cholesterol mass was reduced by approximately 70%. In contrast, the cellular cholesterolreducing capacity of LgLpA-I was negligible. LgLpA-I inhibited net cholesterol removal from foam cells that was mediated by Md and SmLpA-I and cholesteryl ester production with these particles. These results suggest that Md and SmLpA-I may actively participate in cellular cholesterol removal and cholesterol esterification in plasma and HDL, while LgLpA-I may regulate these functions of Md and SmLpA-I.
Key Words: apoA-Icontaining lipoproteins LCAT LpA-I LpA-I/A-II reverse cholesterol transport
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