Lipid transfer particle-induced transformation of human high density lipoprotein into apolipoprotein A-I-deficient low density particles.

摘要: Incubation of human high density lipoprotein (HDL) particles (density = 1.063-1.21 g/ml) with catalytic amounts Manduca sexta lipid transfer particle (LTP) resulted in alteration the distribution HDL protein such that original were transformed into new an equilibrium 1.05 g/ml. Concomitantly, substantial recovered bottom fraction gradient. The LTP-induced was dependent on LTP concentration and incubation time. Electrophoretic analysis revealed lower contained apolipoprotein A-II (apoA-II) as major apoprotein component while nearly all apoA-I fraction. Lipid substrate product fractions apoA-I-rich devoid (less than 1%, w/w). originally associated low density, apoA-II-rich, fraction, ratios individual classes same control HDL. Electron microscopy gel permeation chromatography experiments population comprised larger size (19.7 +/- 1.4-nm diameter) (10.6 diameter). results suggest facilitated net between altered migration occurred donor disintegrated. Similar obtained when HDL3 or HDL2 subclasses employed substrates for LTP. surface area to core volume ratio larger, compared requires there be a decrease total exposed lipid/water interface which stabilization by apolipoprotein. Selective displacement apoA-II apoC, due their greater binding affinity, dictates is preferentially lost from therefore lipid-free apoprotein. Thus, it conceivable structural arrangement components isolated plasma may not represent most thermodynamically stable protein.