Estradiol reduces basal and cytokine induced monocyte adhesion to endothelial cells.
Estradiol reduces basal and cytokine induced monocyte adhesion to endothelial cells.
复制标题
雌二醇减少基础和细胞因子诱导的单核细胞与内皮细胞的粘附。
DOI：
10.1016/s0378-5122(01)00301-2
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发表时间：
2002
期刊：
影响因子：
4.9
通讯作者：
StClair,RichardW
中科院分区：
文献类型：
--
作者：
Mikkola,TomiS;StClair,RichardW
目的探讨在细胞因子诱导或不诱导的情况下，17β-雌二醇（E2）对单核细胞与人主动脉内皮细胞（HAECs）结合的影响。方法在单核细胞粘附试验之前，在有或没有E2的情况下，将融合的HAECs单层孵育48 h。在使用细胞因子的研究中，在最后24或4 h向培养基中加入1 ng/ml肿瘤坏死因子-α（TNF-α）、20 U/ml白细胞介素-1 β（IL-1β）或两者。对于单核细胞粘附的测量，3 H-胸苷标记的人THP-1单核细胞（4× 105个细胞/孔）加入到HAEC的汇合单层中，并在37 ℃下孵育90分钟。通过温和洗涤除去未结合的THP-1细胞，结果用E2预处理HAECs 48 h后，THP-1与HAECs的基础粘附能力明显降低，而THP-1与HAECs的基础粘附能力明显降低。1个细胞平均减少28%。当加入细胞因子4小时时，雌激素显著降低了30-35%的马槟榔诱导的粘附。当细胞因子作用时间延长至24 h时，E2预处理HAECs对THP-1细胞粘附无影响。由于单核细胞与血管内皮细胞的粘附是动脉粥样硬化发病机制的初始步骤之一，因此E2可能通过在动脉粥样硬化形成的早期阶段减少单核细胞与内皮细胞的结合来介导血管保护。
ObjectiveTo investigate the effect of 17β-estradiol (E2) on binding of monocytes to human aortic endothelial cells (HAECs) with or without cytokine induction.MethodsConfluent monolayers of HAECs were incubated with or without E2for 48 h prior to the monocyte adhesion assay. In studies with cytokines, 1 ng/ml tumor necrosis factor-α (TNF-α), 20 U/ml interleukin-1β (IL-1β) or both were added to the culture medium for the final 24 or 4 h. For the measurement of monocyte adhesion,3H-thymidine labeled human THP-1 monocytes (4×105cells per well) were added to the confluent monolayer of HAECs and incubated at 37°C for 90 min. The unbound THP-1 cells were removed by gentle washing, and bound cells were digested with NaOH and quantified by measuring radioactivity.ResultsWhen HAECs were pretreated for 48 h with E2the basal adhesion of THP-1 cells was reduced by an average of 28%. Estrogen significantly reduced cytokine-induced adhesion by 30–35% when the cytokines were added for 4 h. When the cytokine treatment was prolonged to 24 h, pretreatment of HAECs with E2had no effect on THP-1 cell adhesion.ConclusionsE2reduces basal and short-term cytokine induced monocyte binding to HAECs. Since monocyte adhesion to vascular endothelial cells is one of the initial steps in the pathogenesis of atherosclerosis, E2may mediate vascular protection by reducing monocyte-endothelial cell binding in the early stages of atherogenesis.