C-reactive protein–mediated low density lipoprotein uptake by macrophages: implications for atherosclerosis
TP Zwaka, V Hombach, J Torzewski - Circulation, 2001 - Am Heart Assoc
TP Zwaka, V Hombach, J Torzewski
Circulation, 2001•Am Heart AssocBackground—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 …
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 …
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.
Am Heart Assoc