Effects of oxidized LDL on mononuclear phagocytes: inhibition of induction of four inflammatory cytokine gene RNAs, release of NO, and cytolysis of tumor cells.
Effects of oxidized LDL on mononuclear phagocytes: inhibition of induction of four inflammatory cytokine gene RNAs, release of NO, and cytolysis of tumor cells.
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氧化LDL对单核吞噬细胞的影响：抑制四种炎症细胞因子基因RNA的诱导、NO的释放和肿瘤细胞的细胞溶解。
DOI：
10.1002/jlb.57.3.427
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发表时间：
1995
影响因子：
5.5
通讯作者：
Adams,DO
中科院分区：
文献类型：
--
作者：
Thai,SF;Lewis,JG;Williams,RB;Johnson,SP;Adams,DO
动脉粥样硬化发展的关键步骤是氧化低密度脂蛋白（LDL）与单核吞噬细胞的相互作用。氧化LDL以及乙酰LDL通过清道夫受体家族被巨噬细胞迅速摄取。我们报道，脂多糖（LPS）刺激的巨噬细胞的北方印迹分析表明，氧化LDL处理的巨噬细胞具有明显较低的MCP-1、TNF-α、IL-1α和KC基因特异性mRNA水平。相比之下，在氧化LDL有效的剂量下，乙酰LDL不会抑制这些基因。无论LDL在Cu 2+或Fe 2+存在下被氧化，都观察到类似的效果。当使用马来酰化牛血清白蛋白（BSA）作为刺激剂时，也会发生这种抑制，BSA也会被巨噬细胞上的一种或多种清道夫受体清除。Fe ~（2+）或Cu ~（2+）氧化的LDL抑制LPS引发的一氧化氮释放，抑制马来酰化BSA或LPS引发的肿瘤细胞直接溶解。总之，所提供的数据表明，氧化LDL抑制几种重要基因RNA以及表征炎症和完全活化的巨噬细胞的发展的功能标志物的诱导。57：427-433; 1995.
A critical step in development of atherosclerosis is the interaction of oxidized low-density lipoprotein (LDL) with mononuclear phagocytes. Oxidized LDL, as well as acetyl-LDL, is rapidly taken up into macrophages via a family of scavenger receptors. We report that macrophages treated with oxidized LDL have markedly lower levels of mRNA specific for the genes MCP-1, TNF-α, IL-1α, and KC as measured by Northern blot analyses of lipopolysaccharide (LPS)-stimulated macrophages. By contrast, acetyl-LDL does not inhibit these genes at the doses at which oxidized-LDL is effective. Similar effects are observed whether the LDL is oxidized in the presence of Cu2+or of Fe2+. Such inhibition also occurs when maleylated bovine serum albumin (BSA), which also clears by one or more scavenger receptors on macrophages, is used as the stimulant. Fe2+or Cu2+oxidized LDL inhibits release of nitric oxide when triggered by LPS and direct cytolysis of tumor cells when triggered by maleylated BSA or LPS. Taken together, the data presented indicate that oxidized LDL inhibits induction of several important gene RNAs as well as functional markers that characterize the development of inflammatory and fully activated macrophages.J. Leukoc. Biol. 57: 427–433; 1995.