Uptake of Radiolabeled and Colloidal Gold–Labeled Chyle Chylomicrons and Chylomicron Remnants by Rat Platelets In Vitro

Abstract

Abstract This study examined the uptake of chyle chylomicrons (CMs) and chylomicron remnants (CMRs) by rat platelets in vitro. CMs and CMRs were doubly labeled with [ 3 H]arachidonate ([ 3 H]-20:4) and [ 14 C]cholesterol and were incubated with platelets for up to 4 hours. A significant uptake (binding and/or internalization) of CMs by the platelets occurred, as indicated by the parallel increase of [ 3 H]20:4 and [ 14 C]cholesterol in platelets with incubation time. Addition of unlabeled CMs, VLDLs, LDLs, and HDLs decreased the uptake of labeled CMs. The competition experiments suggested that there is both a saturable binding and a nonspecific uptake of CMs. During incubation with CMs, the proportion of [ 3 H]20:4 in phospholipids decreased and that in 1,2-x-diacylglycerol increased. The data indicated that a phospholipase C–mediated degradation of phosphatidylcholine and phosphatidylethanolamine occurred, whereas [ 3 H]20:4 in triglyceride and 14 C in cholesteryl ester did not change. Electron microscopic studies after incubation with colloidal gold–labeled CMs (CM-Au’s) demonstrated an accumulation of CM-Au particles in the open canalicular system of the platelets. Some CM-Au particles were localized in cytoplasmic vacuoles that were not stained by ruthenium red. Some CM-Au’s or free gold particles were in vacuoles that showed acid phosphatase activity, indicating that some true endocytosis of CM occurred. The uptake of [ 3 H]-20:4– and [ 14 C]cholesterol-labeled CMRs was low compared with the uptake of CMs. After incubation with colloidal gold–labeled CMRs (CMR-Au’s), only a few platelets contained CMR-Au in their open canalicular systems, and no CMR-Au particles were seen in the cytoplasm or in acid phosphatase–positive vacuoles. Rat platelets can thus interact with CMs by a process that leads to a sequestration in the open canalicular system and endocytosis and a net degradation of CM phospholipids. The conversion of CMs to CMRs counteracts this interaction.