Downregulation of microglial activation by apolipoprotein E and apoE-mimetic peptides
Downregulation of microglial activation by apolipoprotein E and apoE-mimetic peptides
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DOI：
10.1006/exnr.2001.7541
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发表时间：
2001-01-01
影响因子：
5.3
通讯作者：
Bennett, ER
中科院分区：
文献类型：
--
作者：
Laskowitz, DT;Thekdi, AD;Bennett, ER
载脂蛋白E在急性脑损伤和AZzheimer病的风险恢复中起着重要作用。我们证明，生物相关浓度的载脂蛋白E以剂量依赖的方式抑制小胶质细胞的激活和释放肿瘤坏死因子α和一氧化氮。来自apoE受体结合区的多肽模拟完整蛋白的作用，而apoE残基146-149的缺失会取消多肽的生物活性。这些结果与载脂蛋白E通过结合特定的细胞表面受体来调节小胶质细胞功能的假说是一致的，并且载脂蛋白E在中枢神经系统的免疫调节作用可能是其在急慢性神经系统疾病中的作用。(C)2001年学术出版社。
Apolipoprotein E plays an important role in recovery from acute brain injury and risk of developing AZzheimer's disease. We demonstrate that biologically relevant concentrations of apoE suppress microglial activation and release of TNF alpha and NO in a dose-dependent fashion. Peptides derived from the apoE receptor-binding region mimic the effects of the intact protein, whereas deletion of apoE residues 146-149 abolishes peptide bioactivity. These results are consistent with the hypothesis that apoE modulates microglial function by binding specific cell surface receptors and that the immunomodulatory effects of apoE in the central nervous system may account for its role in acute and chronic neurological disease. (C) 2001 Academic Press.