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首页> 外文期刊>Biochemistry >Macrophage Scavenger Receptor A Mediates Adhesion to Apolipoproteins A-I and E
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Macrophage Scavenger Receptor A Mediates Adhesion to Apolipoproteins A-I and E

机译：巨噬细胞清道夫受体A介导对载脂蛋白A-I和E的粘附。

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Macrophage scavenger receptor A (SR-A) is a multifunctional, multiligand pattern recognitionnreceptor with roles in innate immunity, apoptotic cell clearance, and age-related degenerative pathologies,nsuch as atherosclerosis and Alzheimer’s disease. Known endogenous SR-A ligands are polyanionic andninclude modified lipoproteins, advanced glycation end products, and extracellular matrix proteins. No nativenplasma ligands have been identified, but it is known that SR-A recognition of unidentified serumcomponentsnmediates integrin-independent macrophage adhesion, which may drive chronic local inflammation. In thisnstudy, we used a high-throughput fractionation and screening method to identify novel endogenous SR-Anligands that may mediate macrophage adhesion. SR-A was found to recognize the exchangeable apolipo-nproteins A-I and E (apo A-I and apo E, respectively) in both lipid-free and lipid-associated form, suggestingnthe shared amphipathic R-helix as a potential recognition motif. Adhesion of RAW 264.7 macrophagesnto surfaces coated with apo A-I and apo E4 proved to be integrin-independent and could be blocked by anti-nSR-A antibodies. The presence of apo A-I and apo E in pathological deposits, such as atherosclerotic lesionsnand neurotoxic Alzheimer’s plaques, suggests a possible contribution of SR-A-dependent adhesion ofnmacrophages to an inflammatory microenvironment.
机译：巨噬细胞清除剂受体A（SR-A）是一种多功能，多配体模式识别受体，在先天免疫，凋亡细胞清除以及与年龄有关的退化性疾病（如动脉粥样硬化和阿尔茨海默氏病）中起作用。已知的内源性SR-A配体是聚阴离子，并且包括修饰的脂蛋白，高级糖基化终产物和细胞外基质蛋白。尚未鉴定出原生质体配体，但已知未鉴定的血清成分的SR-A识别介导了不依赖整联蛋白的巨噬细胞粘附，这可能导致慢性局部炎症。在这项研究中，我们使用了高通量分级分离和筛选方法，以鉴定可能介导巨噬细胞粘附的新型内源性SR-配体。发现SR-A以无脂质和脂质相关的形式识别可交换的载脂蛋白n-A和E（分别为apo A-I和apo E），表明共享的两亲R-螺旋是潜在的识别基序。 RAW 264.7巨噬细胞对涂有载脂蛋白A-1和载脂蛋白E4的表面的粘附被证明是整联蛋白独立的，并且可以被抗nSR-A抗体阻断。诸如动​​脉粥样硬化病变和神经毒性阿尔茨海默氏斑块等病理性沉积物中存在载脂蛋白A-I和载脂蛋白E，这表明巨噬细胞依赖SR-A的粘附对炎性微环境的可能贡献。

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