CD36 and proteoglycan-mediated pathways for (n-3) fatty acid enriched triglyceride-rich particle blood clearance in mouse models in vivo and in peritoneal macrophages in vitro.

摘要: Because the mechanisms of (n-3) fatty acid-enriched triglyceride-rich particle [(n-3)-TGRP] uptake are not well characterized, we questioned whether (n-3)-TGRP removed via "nonclassical" pathways, e.g., pathways other than an LDL receptor and/or involving apolipoprotein E (apoE). Chylomicron-sized model labeled with [ 3 H]cholesteryl ether were injected into wild-type (WT) and CD36 knockout (CD36-/-) mice at low, nonsaturating high, saturating doses. Blood clearance was determined by calculating fractional catabolic rates. At doses, blood slower in CD36-/- relative to WT mice, suggesting that part contributes uptake. To further examine potential nonclassical peritoneal-elicited macrophages from incubated presence apoE, lactoferrin, sodium chlorate. Cellular measured test roles apoE-mediated proteoglycans. ApoE-mediated compensated for defective cells. Lactoferrin decreased apoE. Inhibition cell proteoglycan synthesis chlorate reduced both groups macrophages, effects independent We conclude although is involved, it primary contributor (n-3)-TGRP. The removal likely relies more on such as proteoglycan-mediated pathways.