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糖基化终产物(AGE)修饰蛋白及其与动脉粥样硬化的潜在相关性。

Advanced Glycation End Products (AGE)-Modified Proteins and Their Potential Relevance to Atherosclerosis.

机构信息

Department of Biochemistry, Kumamoto University School of Medicine,Kumamoto 860,Japan.

出版信息

Trends Cardiovasc Med. 1996 Jul;6(5):163-8. doi: 10.1016/1050-1738(96)00050-3.

DOI:10.1016/1050-1738(96)00050-3
PMID:21232291
Abstract

Modification of proteins by long-term incubation with glucose leads, through the formation of early products such as Schiff base and Amadori rearrangement products, to the formation of advanced glycation end products (AGE). AGE-modified proteins are characterized physicochemically by fluorescence, brown coloration, and intramolecular or intermolecular cross-linking. Biologically, they are specifically recognized by the AGE receptors of the cell surface membrane. Recent studies have provided evidence for the involvement of AGE proteins in atherosclerosis. First, in vitro experiments using Chinese hamster ovary cells overexpressing the macrophage scavenger receptor (MSR) and peritoneal macrophages from MSR-knockout mice demonstrated that MSR plays a major role as the AGE receptor in the endocytotic uptake of AGE by macrophages. Second, immunohistochemical studies using anti-AGE antibody and anti-MSR antibody revealed the presence of AGE proteins in human atherosclerotic lesions in arterial walls. Because MSR is closely associated with the formation of early atherosclerotic lesions, these results suggest a potential role played by AGE proteins or their interaction with MSR in the atherosclerotic process. (Trends Cardiovasc Med 1996;6:163-168).

摘要

经长期与葡萄糖孵育修饰的蛋白质,通过形成早期产物,如 Schiff 碱和 Amadori 重排产物,导致晚期糖基化终末产物(AGE)的形成。AGE 修饰的蛋白质在物理化学上的特征是荧光、褐色着色、以及分子内或分子间的交联。在生物学上,它们被细胞表面膜上的 AGE 受体特异性识别。最近的研究为 AGE 蛋白在动脉粥样硬化中的作用提供了证据。首先,使用过表达巨噬细胞清道夫受体(MSR)的中国仓鼠卵巢细胞和来自 MSR 基因敲除小鼠的腹腔巨噬细胞进行的体外实验表明,MSR 作为 AGE 受体在巨噬细胞对 AGE 的内吞摄取中起主要作用。其次,使用抗 AGE 抗体和抗 MSR 抗体的免疫组织化学研究揭示了 AGE 蛋白在人动脉壁动脉粥样硬化病变中的存在。因为 MSR 与早期动脉粥样硬化病变的形成密切相关,这些结果表明 AGE 蛋白或其与 MSR 的相互作用在动脉粥样硬化过程中可能发挥作用。(趋势心血管医学 1996 年;6:163-168)。

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