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Published on: October 12, 2017
CD36 is a receptor for oxidized high density lipoprotein: implications for the development of atherosclerosis
Rick F Thorne1, Nizar M Mhaidat, Kylie J Ralston
1Cancer Research Unit, School of Biomedical Science, Faculty of Health, The University of Newcastle, NSW 2308, Australia. Rick.Thorne@newcastle.edu.au
Insights
Macrophage scavenger receptor CD36 facilitates lipid uptake from oxidized high-density lipoprotein (HDL), contributing to atherosclerotic plaque formation. This selective uptake mechanism highlights CD36
Area of Science:
- Molecular Biology
- Cardiovascular Research
- Cell Biology
Background:
- Atherosclerotic plaque formation involves excessive cholesterol ester deposition.
- Tissue macrophages in arterial intima play a critical role in atherogenesis.
- Lipoprotein modification, particularly oxidation, is implicated in plaque development.
Purpose of the Study:
- To investigate the role of the macrophage scavenger receptor CD36 in lipid uptake from modified lipoproteins.
- To determine if CD36 mediates lipid uptake from oxidized high-density lipoprotein (oxHDL).
- To compare the uptake mechanisms of oxHDL with other lipoproteins.
Main Methods:
- Utilized a transfection system with two human cell lines.
- Assessed lipid uptake mediated by the macrophage scavenger receptor CD36.
- Compared uptake from native HDL, low-density lipoprotein (LDL), and Cu(2+)-oxidized HDL (oxHDL).
Main Results:
- CD36 selectively mediated lipid uptake from Cu(2+)-oxidized HDL, but not from native HDL or LDL.
- The uptake of oxHDL via CD36 showed similarities to CD36-dependent oxidized LDL uptake.
- Macrophage CD36 binding and internalization of oxHDL were demonstrated.
Conclusions:
- The macrophage scavenger receptor CD36 plays a specific role in the uptake of oxidized HDL.
- CD36-mediated uptake of oxHDL may contribute significantly to the development of atherosclerotic plaques (atheroma).
- Targeting CD36 could be a potential strategy for managing atherosclerosis.
Abstract:
Atherosclerotic plaques result from the excessive deposition of cholesterol esters derived from lipoproteins and lipoprotein fragments. Tissue macrophage within the intimal space of major arterial vessels have been shown to play an important role in this process. We demonstrate in a transfection system using two human cell lines that the macrophage scavenger receptor CD36 selectively elicited lipid uptake from Cu(2+)-oxidized high density lipoprotein (HDL) but not from native HDL or low density lipoprotein (LDL). The uptake of oxHDL displayed morphological and biochemical similarities with the CD36-dependent uptake of oxidized LDL. CD36-mediated uptake of oxidized HDL by macrophage may therefore contribute to atheroma formation.
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