Suzuki H, Kurihara Y, Takeya M, Kamada N, Kataoka M, Jishage K, Sakaguchi H, Kruijt J K, Higashi T, Suzuki T, van Berkel T J, Horiuchi S, Takahashi K, Yazaki Y, Kodama T
Exploratory Research Laboratory, Chugai Pharmaceutical Co. Ltd., Shizuoka, Japan.
J Atheroscler Thromb. 1997;4(1):1-11. doi: 10.5551/jat1994.4.1.
Both type I and type II MSRs are integral membrane proteins containing a collagenous domain and elicit an extraordinarily wide range of ligand binding capability. They were found during the search for the molecule(s) responsible for the accumulation of modified LDL during atherogenesis. However, all prior the evidence relating to their physiological and pathophysiological roles in vivo had been indirect. Targeted disruption of the MSR gene results in a reduction in the size of atherosclerotic lesions in an apo E deficient animal. Macrophages from MSR deficient mice exhibit a marked decrease in modified LDL uptake in vitro, whereas modified LDL clearance from plasma remains normal, suggesting that there are alternative mechanisms for the uptake of modified LDL from the circulation. In addition, MSR knockout mice are more susceptible to L. monocytogenes and HSV-1 infection, indicating a role for MSR in host defense against various pathogens.
I型和II型巨噬细胞清道夫受体（MSR）均为整合膜蛋白，含有一个胶原结构域，具有极其广泛的配体结合能力。它们是在寻找动脉粥样硬化形成过程中负责修饰低密度脂蛋白（LDL）蓄积的分子时被发现的。然而，此前所有关于它们在体内生理和病理生理作用的证据都是间接的。MSR基因的靶向破坏导致载脂蛋白E缺乏动物的动脉粥样硬化病变尺寸减小。来自MSR缺陷小鼠的巨噬细胞在体外对修饰LDL的摄取显著减少，而血浆中修饰LDL的清除仍保持正常，这表明存在从循环中摄取修饰LDL的替代机制。此外，MSR基因敲除小鼠对单核细胞增生李斯特菌和单纯疱疹病毒1型感染更易感，表明MSR在宿主抵御各种病原体中发挥作用。
