Abstract
Backgroundphospholipid transfer protein (PLTP) plays important roles in lipoprotein metabolism and atherosclerosis and is expressed by macrophages and macrophage foam cells (MFCs). The aim of the present study was to determine whether the major protein from HDL, apoA-I, affects PLTP derived from MFCs.Resultsas cell model we used human THP-1 monocytes incubated with acetylated LDL, to generate MFC. The addition of apoA-I to the cell media increased apoE secretion from the cells, in a concentration dependent fashion, without affecting cellular apoE levels. In contrast, apoA-I had no effect on PLTP synthesis and secretion, but strongly induced the PLTP activity in the media. ApoA-I also increased phospholipid transfer activity of PLTP isolated from human plasma. This effect was dependent on apoA-I concentration but independent on apoA-I lipidation status. ApoE, ApoA-II and apoA-IV, but not immunoglobulins or bovine serum albumin, also increased PLTP activity. We also report that apoA-I protects PLTP from heat inactivation.ConclusionapoA-I enhances the phospholipid transfer activity of PLTP secreted from macrophage foam cells without affecting the PLTP mass.
Highlights
Atherosclerosis is an inflammatory disorder in the artery wall caused by the accumulation of atherogenic lipoproteins such as low density lipoproteins (LDL) and triglyceride rich remnant lipoproteins
In the present study we have investigated the effect of exogenous human apoA-I on the synthesis and secretion of phospholipid transfer protein (PLTP) from human macrophage foam cells
The macrophages were loaded by incubating them in the presence of 25 μg of protein/ well of acetylated LDL (AcLDL) in RPMI 1640 supplemented with 5% (v/v) fetal bovine lipoprotein deficient serum (LPDS), 10 mM Hepes, pH 7.4, and penicillin/ streptomycin for 48 h
Summary
Atherosclerosis is an inflammatory disorder in the artery wall caused by the accumulation of atherogenic lipoproteins such as low density lipoproteins (LDL) and triglyceride rich remnant lipoproteins. In the artery wall these lipoproteins are modified and taken up by macrophages. This sterol loading of the macrophages promotes the formation of macrophage foam cells (MFCs) essential constituents of human atherosclerotic lesions [1]. Major efforts are made to develop therapies that will promote removal of cholesterol from lesion foam cells and lead to regression of the atherosclerotic process [2]. Animal studies have shown that high density lipoproteins (HDL) can promote the removal of cholesterol from the arterial wall and transport it to the liver for excretion in a process called reverse cholesterol transport (RCT) [3]. In addition to RCT, HDL has several other protective
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