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Mouse CD36 has opposite effects on LDL and oxidized LDL metabolism in vivo
Vilayphone Luangrath1, Mathieu R Brodeur, David Rhainds
1Département des Sciences Biologiques, Université du Québec à Montréal, C.P. 8888, Succursale Centreville, Montréal, Québec, Canada.
Insights
Cluster of differentiation-36 (CD36) impedes native LDL clearance while promoting oxidized LDL (oxLDL) uptake in mice. This dual role suggests CD36 contributes to atherosclerosis by negatively impacting LDL metabolism.
Area of Science:
- Lipid metabolism
- Atherosclerosis research
- Molecular biology
Background:
- Cluster of differentiation-36 (CD36) is a protein known for binding oxidized low-density lipoproteins (oxLDL) in macrophages, a process linked to atherogenesis.
- The precise physiological role of CD36 in the metabolism of both native LDL and oxLDL remains to be fully elucidated.
Purpose of the Study:
- To define the in vivo physiological role of CD36 in the metabolism of native LDL and oxLDL in mice.
- To investigate the impact of CD36 on LDL and oxLDL clearance and selective uptake pathways.
Main Methods:
- Conducted clearance studies of labeled LDL and oxLDL in wild-type, CD36 knockout (KO), scavenger receptor class B type I (SR-BI) KO, and double KO mice.
- Performed association and degradation assays using primary hepatic cell cultures from wild-type and CD36 KO mice.
Main Results:
- CD36 was found to impede the clearance of native LDL while facilitating the uptake of oxLDL in vivo.
- Neither SR-BI nor CD36 significantly influenced cholesteryl ester (CE) selective uptake from oxLDL.
- CD36, in the absence of SR-BI, demonstrated the ability to selectively uptake CE from native LDL.
Conclusions:
- This study demonstrates for the first time CD36's significant role in in vivo oxLDL uptake in mice.
- CD36's atherogenic potential may stem from its dual action of retarding LDL clearance and promoting oxLDL uptake, negatively affecting overall LDL metabolism.
Objective:
The cluster of differentiation-36 (CD36) is a multifunctional protein which is recognized for its in vitro ability to take up oxidized low-density lipoproteins (oxLDL) in macrophages and is therefore considered atherogenic. It also binds LDL. Our objective was to define the physiological role of CD36 in both native LDL and oxLDL metabolism in mice.
Methods And Results:
Clearance studies of labeled LDL and oxLDL were conducted in wild-type, CD36 knockout (KO), scavenger receptor class B, type I (SR-BI) KO, and SR-BI/CD36 double KO mice. We found that CD36 impedes the disappearance of native LDL and favors that of oxLDL. This was confirmed by association and degradation assays with primary cultures of hepatic cells from wild-type and CD36 KO mice. In addition, our in vivo work indicates that neither SR-BI nor CD36 plays a significant role in cholesteryl esters (CE) selective uptake (SU) from oxLDL, whereas CD36, in absence of SR-BI, can selectively take CE from LDL.
Conclusions:
Our investigation showed for the first time that CD36 plays a significant role in oxLDL uptake in vivo in the mouse. As CD36 also retards LDL clearance, its atherogenic character may also relate to its negative effect on LDL catabolism.
