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Published on: October 12, 2017
C-reactive protein-mediated low density lipoprotein uptake by macrophages: implications for atherosclerosis
T P Zwaka1, V Hombach, J Torzewski
1Internal Medicine II-Cardiology, University of Ulm, Ulm, Germany.
Insights
C-reactive protein (CRP) may help low-density lipoprotein (LDL) deposit in arteries, leading to foam cell formation. Macrophages take up CRP-opsonized LDL via macropinocytosis, contributing to atherosclerosis.
Area of Science:
- Cardiovascular Biology
- Immunology
- Cell Biology
Background:
- Low-density lipoprotein (LDL) and C-reactive protein (CRP) are key cardiovascular risk factors.
- Both LDL and CRP accumulate in arterial walls during atherosclerosis.
- Native LDL does not induce foam cell formation, suggesting a role for other factors.
Purpose of the Study:
- To investigate if C-reactive protein (CRP) opsonizes native LDL for uptake by macrophages.
- To elucidate the mechanism of CRP-mediated LDL uptake by macrophages.
Main Methods:
- Isolation of human monocytes and differentiation into macrophages.
- Assessment of CRP/LDL uptake using immunofluorescent labeling and confocal laser scanning microscopy.
- Investigating the role of the CRP receptor CD32 in CRP/LDL uptake.
Main Results:
- Macrophages readily took up native LDL when coincubated with CRP.
- This uptake occurred via a process called macropinocytosis.
- The CRP receptor CD32 was identified as the mediator of CRP/LDL uptake.
Conclusions:
- CRP opsonizes native LDL, facilitating its uptake by macrophages.
- Macrophage uptake of CRP-opsonized LDL contributes to foam cell formation.
- This mechanism offers a potential explanation for foam cell formation in human atherogenesis.
Background:
LDL and C-reactive protein (CRP) are important cardiovascular risk factors. Both LDL and CRP deposit in the arterial wall during atherogenesis. Stranded LDL is taken up by macrophages, causing foam cell formation. Because native LDL does not induce foam cell formation, we hypothesized that CRP may opsonize native LDL for macrophages.
Methods And Results:
Monocytes were isolated from human blood and transformed into macrophages. CRP/LDL uptake was assessed by immunofluorescent labeling and the use of confocal laser scanning microscopy. Native LDL coincubated with CRP was taken up by macrophages by macropinocytosis. Uptake of the CRP/LDL coincubate was mediated by the CRP receptor CD32.
Conclusions:
We conclude that foam cell formation in human atherogenesis may be caused in part by uptake of CRP-opsonized native LDL.
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