Zwaka T P, Hombach V, Torzewski J
Internal Medicine II-Cardiology, University of Ulm, Ulm, Germany.
Circulation. 2001 Mar 6;103(9):1194-7. doi: 10.1161/01.cir.103.9.1194.
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.
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.
We conclude that foam cell formation in human atherogenesis may be caused in part by uptake of CRP-opsonized native LDL.
低密度脂蛋白（LDL）和C反应蛋白（CRP）是重要的心血管危险因素。在动脉粥样硬化形成过程中，LDL和CRP都会沉积在动脉壁中。滞留的LDL被巨噬细胞摄取，导致泡沫细胞形成。由于天然LDL不会诱导泡沫细胞形成，我们推测CRP可能会使巨噬细胞对天然LDL进行调理吞噬作用。
从人血液中分离单核细胞并将其转化为巨噬细胞。通过免疫荧光标记和共聚焦激光扫描显微镜评估CRP/LDL摄取情况。与CRP共同孵育的天然LDL通过巨吞饮作用被巨噬细胞摄取。CRP/LDL共孵育物的摄取由CRP受体CD32介导。
我们得出结论，人类动脉粥样硬化形成过程中的泡沫细胞形成可能部分是由CRP调理的天然LDL的摄取引起的。
