INDUCTION OF AN ACTIVATION ANTIGEN ON HUMAN-ENDOTHELIAL CELLS-INVITRO
INDUCTION OF AN ACTIVATION ANTIGEN ON HUMAN-ENDOTHELIAL CELLS-INVITRO
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DOI：
10.1002/eji.1830190422
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发表时间：
1989-04-01
影响因子：
5.4
通讯作者：
BUURMAN, WA
中科院分区：
文献类型：
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作者：
LEEUWENBERG, JFM;JEUNHOMME, TMAA;BUURMAN, WA
本研究描述了用白细胞介素1和肿瘤坏死因子- α混合培养的人脐静脉内皮（HUVE）细胞免疫小鼠获得的单克隆抗体ENA1识别的细胞膜蛋白的表达特征。该ENA1抗原也可被脂多糖和酚酯诱导表达。仅在HUVE细胞和人脐动脉内皮细胞上表达，用这些试剂中的一种或混合预处理。在人成纤维细胞、肾上皮细胞或来源于大网膜组织的间皮细胞上，无论是否用上述抗原诱导剂预处理，均未检测到表达。此外，对多形核细胞、外周血淋巴细胞和单核细胞系U937均无反应性。时间过程实验显示ENA1抗原的表达具有时间依赖性。激活剂作用于HUVE细胞5 h后表达量达到最高，5 h后表达量开始下降。mRNA合成抑制剂放线菌素D和蛋白质合成抑制剂环己亚胺可完全阻断诱导表达，表明发生了从头合成。其他药理试剂对诱导ENA1表达无影响。新描述的抗原的假定作用是讨论与目前的知识分子参与免疫细胞在炎症过程中的粘附。
This study describes the expression characteristics of a cell membrane protein recognized by a monoclonal antibody ENA1, which was obtained by immunizing mice with human umbilical vein endothelial (HUVE) cells cultured with a mixture of interleukin 1 and tumor necrosis factor-.alpha.. The expression of this ENA1 antigen could also be induced by lipopolysaccharide and phorbol esters. Expression was only demonstrated on HUVE cells and human umbilical arterial endothelial cells, pretreated with one or with a mixture of these reagents. No expression was detected on human fibroblasts, renal epithelial cells or on mesothelial cells derived from omental tissue, either pretreated or not with the aforementioned inducers of the antigen. Furthermore, no reactivity was observed with either polymorphonuclear cells, peripheral blood lymphocytes or the monocytic cell line U937. Time course experiments revealed that the expression of the ENA1 antigen was time dependent. Maximal expression on HUVE cells was observed after 5 h of incubation with activator, after which a decline in expression occurred. Induction of expression could be completely blocked by the mRNA synthesis inhibitor actinomycin D and the protein synthesis inhibitor cycloheximide, indicating that de novo synthesis occurs. Other pharmacological reagents tested had no effect on the induction of ENA1 expression. The putative role of the newly described antigen is discussed in relation to the current knowledge of molecules involved in adhesion of immune cells in inflammatory processes.