Year: 2002
Type: article
Abstract: To maintain cholesterol (CH) homeostasis, cells must balance de novo synthesis against exogenous uptake of cholesteryl esters (CE) and triglycerides (TG) in lipoprotein particles.The objective of this study was to directly investigate the roles of low-density lipoprotein receptor (LDLR), apolipoprotein E (apoE), and the scavenger receptor CD36 in lysosomal trafficking of lipoproteins.To study the roles of LDLR, apoE, and CD36, LAL null (lal-/-) mice were bred to LDLR null (ldlr-/-) and apoE null (apoE-/-) mice to generate lal-/-;ldlr-/-, lal-/-;apoE-/-, and lal-/-;ldlr-/-;apoE-/-mice.CD36 null (CD36-/-) mice were bred to lal-/-mice to generate lal-/-;CD36-/-mice.Analysis of the CE fatty acids in lal-/-livers indicated that the proportion of linoleate esterified CE decreased with age, 25.6 % (1.5 mos) vs. 19.1 % (5 mos).The absence of LDLR and/or apoE in lal-/mice did not change the histology but produced quantitative decreases in hepatic CH contents, 21.6 % (lal-/-;ldlr-/-), 47.5 % (lal-/-;apoE-/-), and 46.3 % (lal-/-;ldlr-/-;apoE-/-) at 5 mos, and 70.2 % (lal-/-;ldlr-/-), 77.0 % (lal-/-;apoE-/-), and 78.2 % (lal-/-;ldlr-/-;apoE-/-) at 8 mos relative to lal-/-mice.Hepatic TG contents were also decreased relative to lal-/-mice, 48.3 % (lal-/-;ldlr-/-), 74.1 % (lal-/-;apoE-/-), and 51.0 % (lal-/-;ldlr-/-; apoE-/-) at 5 mos, and 71.9 % (lal-/-;ldlr-/-), 14.2 % (lal-/-;apoE-/-), and 34.9 % (lal-/-;ldlr-/-;apoE-/-) at 8 mos.The absence of CD36 in lal-/-mice did not produce histological or quantitative changes in the liver.The results indicate that there is no exclusive pathway for lysosomal trafficking of lipoproteins in the liver.
Author: J. Martin Heur
Institution: University of Cincinnati
Language: English
Subfield: Biochemistry
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W1032157382