de Villiers W J, Fraser I P, Hughes D A, Doyle A G, Gordon S
Sir William Dunn School of Pathology, University of Oxford, UK.
J Exp Med. 1994 Aug 1;180(2):705-9. doi: 10.1084/jem.180.2.705.
Regulation of macrophage scavenger receptor (MSR) activity may be an important determinant of the extent of atherogenesis. The effect of macrophage-colony-stimulating factor (M-CSF) on this pathway was studied using a recently developed monoclonal antibody to murine MSR. M-CSF markedly and selectively increased MSR synthesis in murine macrophages: posttranslationally, the receptor appeared more stable and shifted to a predominantly surface distribution. Functionally, M-CSF enhanced modified lipoprotein uptake and increased divalent cation-independent adhesion in vitro. These results suggest a plausible mechanism whereby M-CSF production in the atheromatous plaque microenvironment could promote the recruitment and retention of mononuclear phagocytes and subsequent foam cell formation.
巨噬细胞清道夫受体（MSR）活性的调节可能是动脉粥样硬化发生程度的一个重要决定因素。使用最近开发的针对小鼠MSR的单克隆抗体研究了巨噬细胞集落刺激因子（M-CSF）对该途径的影响。M-CSF显著且选择性地增加了小鼠巨噬细胞中MSR的合成：在翻译后，受体显得更稳定，并转移到主要位于表面的分布。在功能上，M-CSF增强了修饰脂蛋白的摄取，并增加了体外不依赖二价阳离子的黏附。这些结果提示了一种合理的机制，通过该机制动脉粥样斑块微环境中M-CSF的产生可促进单核吞噬细胞的募集和滞留以及随后的泡沫细胞形成。
