Abstract

BackgroundScavenger receptor BI (SR-BI) is a classic high-density lipoprotein (HDL) receptor, which mediates selective lipid uptake from HDL cholesterol esters (HDL-C). Apolipoprotein M (ApoM), as a component of HDL particles, could influence preβ-HDL formation and cholesterol efflux. The aim of this study was to determine whether SR-BI deficiency influenced the expression of ApoM.MethodsBlood samples and liver tissues were collected from SR-BI gene knockout mice, and serum lipid parameters, including total cholesterol (TC), triglyceride (TG), high and low-density lipoprotein cholesterol (HDL-C and LDL-C) and ApoM were measured. Hepatic ApoM and ApoAI mRNA levels were also determined. In addition, BLT-1, an inhibitor of SR-BI, was added to HepG2 cells cultured with cholesterol and HDL, under serum or serum-free conditions. The mRNA and protein expression levels of ApoM were detected by RT-PCR and western blot.ResultsWe found that increased serum ApoM protein levels corresponded with high hepatic ApoM mRNA levels in both male and female SR-BI−/− mice. Besides, serum TC and HDL-C were also significantly increased. Treatment of HepG2 hepatoma cells with SR-BI specific inhibitor, BLT-1, could up-regulate ApoM expression in serum-containing medium but not in serum-free medium, even in the presence of HDL-C and cholesterol.ConclusionsResults suggested that SR-BI deficiency promoted ApoM expression, but the increased ApoM might be independent from HDL-mediated cholesterol uptake in hepatocytes.

Highlights

  • Scavenger receptor BI (SR-BI) is a classic high-density lipoprotein (HDL) receptor, which mediates selective lipid uptake from HDL cholesterol esters (HDL-C)

  • It has been suggested that Apolipoprotein M (ApoM) is one of the important regulators of cholesterol metabolism and reverse cholesterol transport (RCT), because ApoM-enriched HDL increases the ability of HDL to mobilize cellular cholesterol, and accelerates cholesterol efflux from macrophages in vivo [22]

  • Our results indicated that the absence of SR-BI did up-regulate ApoM expression, both in mRNA and protein levels in SR-BI gene knockout mice (Fig. 2), which suggested SR-BI could regulate expression of ApoM

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Summary

Introduction

Scavenger receptor BI (SR-BI) is a classic high-density lipoprotein (HDL) receptor, which mediates selective lipid uptake from HDL cholesterol esters (HDL-C). High-density lipoprotein (HDL), which is always considered as a protective factor against atherosclerosis, serves as a vehicle for delivering excess cholesterol esters from peripheral tissues or cells to the liver and steroidgenic tissues. Scavenger receptor class B type I (SR-BI) is a physiological high-affinity HDL receptor [1, 2]. ApoM could delay oxidation of low-density lipoprotein cholesterol (LDL-C), influence preβ-HDL formation, mediating the antioxidant effect of HDL and acting as an acceptor of sphingosine-1-phosphate (S1P) [18,19,20,21]. Since SR-BI is a key factor in RCT, this study was designed to investigate whether deficiency of SR-BI could affect the expression of ApoM, as well as its potential mechanisms

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