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Scavenger receptors are a group of receptors that recognize modified low-density lipoprotein[1 ] (LDL) by oxidation or acetylation. This naming is based on a function of cleaning (scavenging): Scavenger receptors widely recognize and uptake macromolecules having a negative charge as well as modified LDL.

Contents

Function

It is thought that scavenger receptors participate in the removal of many foreign substances and waste materials in the living body by extensive ligand specificity and a variety of receptor molecules.

In atherosclerotic lesions, macrophages that express scavenger receptors on their plasma membrane aggressively uptake the oxidized LDL deposited in the blood vessel wall inside and become foam cells, and they secrete various inflammatory cytokines and accelerate the development of atherosclerosis.

Types

Scavenger receptors are categorized into classes A, B, and C according to their structural characteristics.

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Scavenger receptor class A

Scavenger receptors type 1 (SR-A1) and 2 (SR-A2) are trimers with a molecular weight of about 220-250 kDa (the molecular weight of monomeric protein is about 80 kDa). They preferentially bind modified LDL by acetic acid and oxidized LDL. They have a collagen-like domain, which is essential for ligand binding. SR-A1 scavenger receptors have a cysteine-rich domain, which can be found in a series of cell surface receptors and soluble proteins, but SR-A2 do not. Another scavenger receptor class A, MARCO, has collagen-like and cysteine-rich domains.

Scavenger receptor class B

CD36 and scavenger receptor class B1 (SR-B1) are identified as oxidized LDL receptors and classified into class B. Both proteins have two transmembrane domains, and they are concentrated in a specific plasma membrane microdomain, the caveolae. CD36 has been thought to be implicated in cell adhesion, in the phagocytosis of apoptotic cells, and in the metabolism of long-chain fatty acids. SR-B1 can interact not only with oxidized LDL but also with normal LDL and high-density lipoproteins (HDL). Recent studies have indicated that SR-B1 are involved in HDL metabolism.

In experimental mice models of atheroslcerosis, in which the gene for CD36 has been deleted, the mice have a greatly reduced number of atherosclerotic lesions[3].

Others

Some receptors that can bind to oxidized LDL have been discovered.

References

External links


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