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巨噬细胞集落刺激因子选择性增强巨噬细胞清道夫受体的表达及功能。

Macrophage-colony-stimulating factor selectively enhances macrophage scavenger receptor expression and function.

作者信息

de Villiers W J, Fraser I P, Hughes D A, Doyle A G, Gordon S

机构信息

Sir William Dunn School of Pathology, University of Oxford, UK.

出版信息

J Exp Med. 1994 Aug 1;180(2):705-9. doi: 10.1084/jem.180.2.705.

Abstract

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.

摘要

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。

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