Plasma lipoprotein induction and suppression of the generation of cellular procoagulant activity in vitro.
Plasma lipoprotein induction and suppression of the generation of cellular procoagulant activity in vitro.
复制标题
体外血浆脂蛋白诱导和抑制细胞促凝血活性的产生。
DOI：
10.1172/jci110196
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发表时间：
1981
期刊：
影响因子：
--
通讯作者：
Edgington,TS
中科院分区：
文献类型：
--
作者：
Levy,GA;Schwartz,BS;Curtiss,LK;Edgington,TS
在先前的报告中已经证明，生理浓度的分离的人血浆极低密度、中密度和高密度脂蛋白在体外诱导人外周血单核细胞促凝血活性的显著增加，而低密度脂蛋白则没有。在本研究中，通过细胞分级分离和直接细胞学测定将单核细胞鉴定为这种诱导活性的来源，从而将促凝血活性鉴定为单核因子。这些脂蛋白诱导的促凝血单核因子的产生完全依赖于淋巴细胞的存在。已暴露于刺激性脂蛋白的分离的淋巴细胞可以诱导单核细胞产生促凝血活性，而来自脂蛋白刺激的淋巴细胞的培养基、淋巴细胞的匀浆或其他细胞（如血小板）都不能替代这种需要。刺激性脂蛋白与淋巴细胞的相互作用迅速，在30分钟内完成，在4° C或37°C下同样有效。低密度脂蛋白没有刺激淋巴细胞诱导单核细胞促凝血活性，但积极抑制生产的促凝血单核因子诱导的每一个刺激性脂蛋白，以及细菌脂多糖。单核细胞被鉴定为对低密度脂蛋白抑制敏感的细胞，并且未观察到对淋巴细胞触发的抑制。血浆脂蛋白与淋巴细胞和单核细胞在体外的相互作用的这些观察介绍了两个新的调节事件，血浆脂蛋白影响细胞的功能，并定义了一个调节网络，某些脂蛋白类触发淋巴细胞，这反过来又可以诱导单核细胞表达促凝血活性。只有后一阶段受到生理浓度的低密度脂蛋白的脂蛋白抑制。图片
Isolated human plasma very low density, intermediate density, and high density lipo-proteins at physiologic concentrations have been demonstrated in the preceding report to induce significant increases in the procoagulant activity of human peripheral blood mononuclear cells in vitro, whereas low density lipoprotein did not. The monocyte was identified in this study by cellular fractionation and by direct cytologic assays as the source of this inducible activity, thus identifying the procoagulant activity as a monokine. The generation of these lipoprotein-induced procoagulant monokines was entirely dependent upon the presence of lymphocytes. Isolated lymphocytes that had been exposed to the stimulatory lipoproteins could induce monocytes to produce the procoagulant activity, whereas neither the culture medium from lipoprotein-stimulated lymphocytes, homogenates of lymphocytes, nor other cells such as platelets could substitute for this requirement. The interaction of the stimulatory lipoproteins with lymphocytes was rapid, reaching completion within 30 min, and was equally effective at either 4° or 37°C. Low density lipoprotein did not stimulate lymphocytes to induce monocyte procoagulant activity, but did actively suppress the production of the procoagulant monokines induced by each of the stimulatory lipoproteins, as well as bacterial lipopolysaccharide. The monocyte was identified as the cell sensitive to low density lipoprotein suppression, and no suppression of lymphocyte triggering was observed. These observations on the interaction of plasma lipoproteins with lymphocytes and monocytes in vitro introduce two new regulatory events by which plasma lipoproteins influence the function of cells, and define a regulatory network by which certain lipoprotein classes trigger lymphocytes, which can in turn induce monocytes to express procoagulant activity. Only this latter phase is subject to lipoprotein suppression by physiologic concentrations of low density lipoprotein.Images