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粒细胞-巨噬细胞集落刺激因子对人单核细胞黏附的调节

Regulation of human monocyte adherence by granulocyte-macrophage colony-stimulating factor.

作者信息

Gamble J R, Elliott M J, Jaipargas E, Lopez A F, Vadas M A

机构信息

Division of Human Immunology, Institute of Medical and Veterinary Science, Adelaide, South Australia.

出版信息

Proc Natl Acad Sci U S A. 1989 Sep;86(18):7169-73. doi: 10.1073/pnas.86.18.7169.

DOI:10.1073/pnas.86.18.7169
PMID:2674950
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC298017/
Abstract

Recombinant human granulocyte-macrophage colony-stimulating factor (GM-CSF) was found to increase the adherence of purified peripheral blood monocytes to plastic surfaces and to monolayers of human umbilical vein endothelial cells. With plastic surfaces as a model 9-hr culture with GM-CSF was necessary for enhancement, and maximum levels were obtained after 24-hr stimulation. GM-CSF-stimulated adherence must require new RNA and protein synthesis because actinomycin D and cycloheximide abolished existing adherence and prevented further monocyte attachment. Interestingly, shorter incubations (1-2 hr) with cycloheximide increased adherence, suggesting a labile inhibitor. Formaldehyde fixation of monocytes but not of human vein endothelial cells abolished adherence, indicating the need for actively metabolizing monocytes. Thus, a hemopoietic growth factor, responsible for the proliferation and differentiation of monocytes, can also alter their adhesive characteristics. These observations may have important implications in pathological situations and in the in vivo use of GM-CSF.

摘要

重组人粒细胞巨噬细胞集落刺激因子(GM-CSF)被发现可增加纯化的外周血单核细胞对塑料表面以及人脐静脉内皮细胞单层的黏附。以塑料表面为模型,GM-CSF处理9小时的培养对于增强黏附是必要的,并且在24小时刺激后可达到最高水平。GM-CSF刺激的黏附必定需要新的RNA和蛋白质合成,因为放线菌素D和环己酰亚胺可消除现有的黏附并阻止单核细胞进一步附着。有趣的是,用环己酰亚胺进行较短时间(1-2小时)的孵育会增加黏附,提示存在一种不稳定的抑制剂。用甲醛固定单核细胞而非人静脉内皮细胞可消除黏附,这表明需要有活跃代谢的单核细胞。因此,一种负责单核细胞增殖和分化的造血生长因子,也可改变其黏附特性。这些观察结果可能在病理情况下以及GM-CSF的体内应用中具有重要意义。

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Studies on the pathogenesis of atherosclerosis. I. Adhesion and emigration of mononuclear cells in the aorta of hypercholesterolemic rats.动脉粥样硬化发病机制的研究。I. 高胆固醇血症大鼠主动脉中单核细胞的黏附和游走
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